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data-props="{"color":"gray","children":["Centro de Investigaciones Biológicas"]}" data-trace="false" data-dom-id="Pill-react-component-90fde579-7eec-4fd1-92a7-4594360f661e"></div> <div id="Pill-react-component-90fde579-7eec-4fd1-92a7-4594360f661e"></div> </a><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="33592395" href="https://www.academia.edu/Documents/in/Bioquimica"><div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Bioquimica"]}" data-trace="false" data-dom-id="Pill-react-component-90f6862a-5bbb-4c4b-8f3c-c92f5de3b4c0"></div> <div id="Pill-react-component-90f6862a-5bbb-4c4b-8f3c-c92f5de3b4c0"></div> </a></div></div></div></div><div class="right-panel-container"><div class="user-content-wrapper"><div class="uploads-container" id="social-redesign-work-container"><div class="upload-header"><h2 class="ds2-5-heading-sans-serif-xs">Uploads</h2></div><div class="documents-container backbone-social-profile-documents" style="width: 100%;"><div class="u-taCenter"></div><div class="profile--tab_content_container js-tab-pane tab-pane active" id="all"><div class="profile--tab_heading_container js-section-heading" data-section="Papers" id="Papers"><h3 class="profile--tab_heading_container">Papers by Luis Peso</h3></div><div class="js-work-strip profile--work_container" data-work-id="99959024"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/99959024/Disruption_of_the_CED_9_center_dot_CED_4_complex_by_EGL_1_is_a_critical_step_for_programmed_cell_death_in_Caenorhabditis_elegans"><img alt="Research paper thumbnail of Disruption of the CED-9 center dot CED-4 complex by EGL-1 is a critical step for programmed cell death in Caenorhabditis elegans" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/99959024/Disruption_of_the_CED_9_center_dot_CED_4_complex_by_EGL_1_is_a_critical_step_for_programmed_cell_death_in_Caenorhabditis_elegans">Disruption of the CED-9 center dot CED-4 complex by EGL-1 is a critical step for programmed cell death in Caenorhabditis elegans</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In the nematode Caenorhabditis elegans, the apoptotic machinery is composed of four basic element...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">In the nematode Caenorhabditis elegans, the apoptotic machinery is composed of four basic elements: the caspase CED-3, the Apaf-1 homologue CED-4, and the Bcl-2 family members CED-9 and EGL-1. The ced-9(n1950) gain-of-function mutation prevents most, if not all, somatic cell deaths in C. elegans. It encodes a CED-9 protein with a glycine-to-glutamate substitution at position 169, which is located within the highly conserved Bcl-2 homology 1 domain, We performed biochemical analyses with the CED-9G169E protein to gain insight into the mechanism of programmed cell death, We find that CED-9G169E retains the ability to bind both EGL-1 and CED-4, although its affinity for EGL-1 is reduced. In contrast to the behavior of wild-type CED-9, the interaction between CED-9G169E and CED-4 is not disrupted by expression of EGL-1. Furthermore, CED-4 and CED-9G169E co-localizes with EGL-1 to the mitochondria in mammalian cells, and expression of EGL-1 does not induce translocation of CED-4 to the c...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="99959024"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="99959024"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 99959024; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=99959024]").text(description); $(".js-view-count[data-work-id=99959024]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 99959024; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='99959024']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 99959024, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=99959024]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":99959024,"title":"Disruption of the CED-9 center dot CED-4 complex by EGL-1 is a critical step for programmed cell death in Caenorhabditis elegans","translated_title":"","metadata":{"abstract":"In the nematode Caenorhabditis elegans, the apoptotic machinery is composed of four basic elements: the caspase CED-3, the Apaf-1 homologue CED-4, and the Bcl-2 family members CED-9 and EGL-1. The ced-9(n1950) gain-of-function mutation prevents most, if not all, somatic cell deaths in C. elegans. It encodes a CED-9 protein with a glycine-to-glutamate substitution at position 169, which is located within the highly conserved Bcl-2 homology 1 domain, We performed biochemical analyses with the CED-9G169E protein to gain insight into the mechanism of programmed cell death, We find that CED-9G169E retains the ability to bind both EGL-1 and CED-4, although its affinity for EGL-1 is reduced. In contrast to the behavior of wild-type CED-9, the interaction between CED-9G169E and CED-4 is not disrupted by expression of EGL-1. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="99959014"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/99959014/Identification_of_a_region_on_hypoxia_inducible_factor_prolyl_4_hydroxylases_that_determines_their_specificity_for_the_oxygen_degradation_domains"><img alt="Research paper thumbnail of Identification of a region on hypoxia-inducible-factor prolyl 4-hydroxylases that determines their specificity for the oxygen degradation domains" class="work-thumbnail" src="https://attachments.academia-assets.com/100910160/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/99959014/Identification_of_a_region_on_hypoxia_inducible_factor_prolyl_4_hydroxylases_that_determines_their_specificity_for_the_oxygen_degradation_domains">Identification of a region on hypoxia-inducible-factor prolyl 4-hydroxylases that determines their specificity for the oxygen degradation domains</a></div><div class="wp-workCard_item"><span>Biochemical Journal</span><span>, 2007</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">HIFs [hypoxia-inducible (transcription) factors] are essential for the induction of an adaptive g...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">HIFs [hypoxia-inducible (transcription) factors] are essential for the induction of an adaptive gene expression programme under low oxygen partial pressure. The activity of these transcription factors is mainly determined by the stability of the HIFα subunit, which is regulated, in an oxygen-dependent manner, by a family of three prolyl 4-hydroxylases [EGLN1–EGLN3 (EGL nine homologues 1–3)]. HIFα contains two, N- and C-terminal, independent ODDs (oxygen-dependent degradation domains), namely NODD and CODD, that, upon hydroxylation by the EGLNs, target HIFα for proteasomal degradation. In vitro studies indicate that each EGLN shows a differential preference for ODDs, However, the sequence determinants for such specificity are unknown. In the present study we showed that whereas EGLN1 and EGLN2 acted upon any of these ODDs to regulate HIF1α protein levels and activity in vivo, EGLN3 only acted on the CODD. With the aim of identifying the region within EGLNs responsible for their diffe...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9bc0fc55b33e1fa58252f1665353c8e5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":100910160,"asset_id":99959014,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/100910160/download_file?st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="99959014"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="99959014"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 99959014; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=99959014]").text(description); $(".js-view-count[data-work-id=99959014]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 99959014; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='99959014']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 99959014, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "9bc0fc55b33e1fa58252f1665353c8e5" } } $('.js-work-strip[data-work-id=99959014]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":99959014,"title":"Identification of a region on hypoxia-inducible-factor prolyl 4-hydroxylases that determines their specificity for the oxygen degradation domains","translated_title":"","metadata":{"abstract":"HIFs [hypoxia-inducible (transcription) factors] are essential for the induction of an adaptive gene expression programme under low oxygen partial pressure. 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class="js-work-strip profile--work_container" data-work-id="91598449"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/91598449/Nod1_an_Apaf_1_like_Activator_of_Caspase_9_and_Nuclear_Factor_%CE%BAB"><img alt="Research paper thumbnail of Nod1, an Apaf-1-like Activator of Caspase-9 and Nuclear Factor-κB" class="work-thumbnail" src="https://attachments.academia-assets.com/94840992/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/91598449/Nod1_an_Apaf_1_like_Activator_of_Caspase_9_and_Nuclear_Factor_%CE%BAB">Nod1, an Apaf-1-like Activator of Caspase-9 and Nuclear Factor-κB</a></div><div class="wp-workCard_item"><span>Journal of Biological Chemistry</span><span>, 1999</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="15411fbdb892423da8cf3f628f86b30f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":94840992,"asset_id":91598449,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/94840992/download_file?st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="91598449"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item 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{"id":91598449,"title":"Nod1, an Apaf-1-like Activator of Caspase-9 and Nuclear Factor-κB","translated_title":"","metadata":{"publisher":"Elsevier BV","ai_title_tag":"Nod1: A Novel Apaf-1-like Regulator of Caspase-9 and NF-kB","grobid_abstract":"Ced-4 and Apaf-1 belong to a major class of apoptosis regulators that contain caspase-recruitment (CARD) and nucleotide-binding oligomerization domains. Nod1, a protein with an NH 2-terminal CARD-linked to a nucleotide-binding domain and a COOH-terminal segment with multiple leucine-rich repeats, was identified. Nod-1 was found to bind to multiple caspases with long prodomains, but specifically activated caspase-9 and promoted caspase-9-induced apoptosis. As reported for Apaf-1, Nod1 required both the CARD and P-loop for function. Unlike Apaf-1, Nod1 induced activation of nuclear factor-kappa-B (NF-B) and bound RICK, a CARDcontaining kinase that also induces NF-B activation. Nod1 mutants inhibited NF-B activity induced by RICK, but not that resulting from tumor necrosis factor-␣ stimulation. Thus, Nod1 is a leucine-rich repeatcontaining Apaf-1-like molecule that can regulate both apoptosis and NF-B activation pathways. Apoptosis, or programmed cell death, is a process that is essential for normal development and homeostasis of multicellular organisms (1-3). Genetic studies in the nematode Caenorhabditis elegans have identified core components of the death machinery, which are conserved in vertebrates, including humans (1-3). One of these, Ced-4, is required for developmental cell death in the worm (1, 2). Ced-4 physically interacts with Ced-3 and promotes the proteolytic activation of the immature Ced-3 caspase into enzymatically active subunits (4-7). Apaf-1, a mammalian homologue of Ced-4, has been identified (8). Both Apaf-1 and Ced-4 are composed of an NH 2-terminal caspase recruitment domain (CARD) 1 linked to a nucleotide-binding domain (NBD), also known as the NB-ARC or NOD domain (3, 8-10). Ced-4 and Apaf-1 self-associate via the NBD, a process that mediates proximity and activation of immature Ced-3/caspase-9 molecules (11-13). The COOH-terminal region of Apaf-1 lacks homology with Ced-4 and is composed of 12 WD-40 repeats (8). In response to certain apoptotic stimuli, cytochrome c is released from the mitochondria and binds to Apaf-1 (8, 14), and in the presence of dATP or ATP, Apaf-1 associates with and activates procaspase-9 (8, 14). Recent analyses of Apaf-1-deficient mice suggest a central role of Apaf-1 in apoptosis induced by chemotherapeutic drugs, ultraviolet radiation, and signals associated with neuronal development (15, 16). Mutant mice deficient in caspase-9 exhibit abnormalities similar, but not identical, to those observed in mice lacking Apaf-1 (17, 18). Unlike C. elegans, mice and humans contain multiple initiator caspases, suggesting that mammalian genomes may contain caspase activators other than Apaf-1. Significantly, Apaf-1 knockout mice lack apparent abnormalities in tissues, such as the thymus, whose appropriate cellular development depends on apoptosis (15, 16). The latter observation suggests the existence of additional Apaf-1like molecules or apoptosis pathways that are Apaf-1-independent. In this study, we identified and characterized Nod1, an Apaf-1-like protein that associates with and regulates procaspase-9. Unlike Apaf-1, however, Nod1 contains leucine-rich repeats (LRRs) and induces NF-B activation.","publication_date":{"day":null,"month":null,"year":1999,"errors":{}},"publication_name":"Journal of Biological Chemistry","grobid_abstract_attachment_id":94840992},"translated_abstract":null,"internal_url":"https://www.academia.edu/91598449/Nod1_an_Apaf_1_like_Activator_of_Caspase_9_and_Nuclear_Factor_%CE%BAB","translated_internal_url":"","created_at":"2022-11-25T12:03:26.350-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":33592395,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":94840992,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/94840992/thumbnails/1.jpg","file_name":"14560.full.pdf","download_url":"https://www.academia.edu/attachments/94840992/download_file?st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Nod1_an_Apaf_1_like_Activator_of_Caspase.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/94840992/14560.full-libre.pdf?1669407211=\u0026response-content-disposition=attachment%3B+filename%3DNod1_an_Apaf_1_like_Activator_of_Caspase.pdf\u0026Expires=1732938997\u0026Signature=DFasQg0sc1j3J2xR-bzN5jH25UBanVtyqmYHZexrqXTuK2efvtwUjuCw-pNetK2sRwdQBJyLYWKSeOQKmxLeT9Zu2zAS4Y23BJq3Tvpj2t0WbcNVaHy2HfPia-oYcwSfuz2fLcPDMJGGCwCQ-AH5PQ0FnYE3-EOBHh4F8bS5lW2U2OtjtbzgvgJUNj8YMUOzolsl1o2SH3INdThVNJuVvEZ7UecWn9LP9GHwIiQGV3lRyoI1FyVKqhHj6P2vSE9DNNDHSmHCslixLL7rj8RC1kT9WiTOXRn4uEhf8ZeFEDJej~6VMOPFriFnmn8BN8Vyjknxdoh7hS-Xqn7MA36CxQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Nod1_an_Apaf_1_like_Activator_of_Caspase_9_and_Nuclear_Factor_κB","translated_slug":"","page_count":9,"language":"en","content_type":"Work","owner":{"id":33592395,"first_name":"Luis","middle_initials":null,"last_name":"Peso","page_name":"LuisPeso","domain_name":"uam","created_at":"2015-08-04T01:22:11.189-07:00","display_name":"Luis Peso","url":"https://uam.academia.edu/LuisPeso"},"attachments":[{"id":94840992,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/94840992/thumbnails/1.jpg","file_name":"14560.full.pdf","download_url":"https://www.academia.edu/attachments/94840992/download_file?st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Nod1_an_Apaf_1_like_Activator_of_Caspase.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/94840992/14560.full-libre.pdf?1669407211=\u0026response-content-disposition=attachment%3B+filename%3DNod1_an_Apaf_1_like_Activator_of_Caspase.pdf\u0026Expires=1732938997\u0026Signature=DFasQg0sc1j3J2xR-bzN5jH25UBanVtyqmYHZexrqXTuK2efvtwUjuCw-pNetK2sRwdQBJyLYWKSeOQKmxLeT9Zu2zAS4Y23BJq3Tvpj2t0WbcNVaHy2HfPia-oYcwSfuz2fLcPDMJGGCwCQ-AH5PQ0FnYE3-EOBHh4F8bS5lW2U2OtjtbzgvgJUNj8YMUOzolsl1o2SH3INdThVNJuVvEZ7UecWn9LP9GHwIiQGV3lRyoI1FyVKqhHj6P2vSE9DNNDHSmHCslixLL7rj8RC1kT9WiTOXRn4uEhf8ZeFEDJej~6VMOPFriFnmn8BN8Vyjknxdoh7hS-Xqn7MA36CxQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":18520,"name":"Biological Chemistry","url":"https://www.academia.edu/Documents/in/Biological_Chemistry"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":50841,"name":"Caspases","url":"https://www.academia.edu/Documents/in/Caspases"},{"id":74780,"name":"Mutation","url":"https://www.academia.edu/Documents/in/Mutation"},{"id":117643,"name":"Biological","url":"https://www.academia.edu/Documents/in/Biological"},{"id":123418,"name":"NF-kappa B","url":"https://www.academia.edu/Documents/in/NF-kappa_B"},{"id":181569,"name":"Proteins","url":"https://www.academia.edu/Documents/in/Proteins"},{"id":247477,"name":"Caspase","url":"https://www.academia.edu/Documents/in/Caspase"},{"id":260118,"name":"CHEMICAL SCIENCES","url":"https://www.academia.edu/Documents/in/CHEMICAL_SCIENCES"},{"id":809881,"name":"Amino Acid Sequence","url":"https://www.academia.edu/Documents/in/Amino_Acid_Sequence"},{"id":1639402,"name":"nuclear factor kappa B","url":"https://www.academia.edu/Documents/in/nuclear_factor_kappa_B"},{"id":1954157,"name":"Apoptotic Protease Activating Factor-1","url":"https://www.academia.edu/Documents/in/Apoptotic_Protease_Activating_Factor-1"},{"id":2467566,"name":"Molecular Sequence Data","url":"https://www.academia.edu/Documents/in/Molecular_Sequence_Data"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":26386654,"url":"https://api.elsevier.com/content/article/PII:S0021925819731275?httpAccept=text/xml"}]}, dispatcherData: dispatcherData }); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="79877823"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/79877823/ERK2_but_Not_ERK1_Mediates_Acquired_and_De_novo_Resistance_to_Imatinib_Mesylate_Implication_for_CML_Therapy"><img alt="Research paper thumbnail of ERK2, but Not ERK1, Mediates Acquired and “De novo” Resistance to Imatinib Mesylate: Implication for CML Therapy" class="work-thumbnail" src="https://attachments.academia-assets.com/86444928/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/79877823/ERK2_but_Not_ERK1_Mediates_Acquired_and_De_novo_Resistance_to_Imatinib_Mesylate_Implication_for_CML_Therapy">ERK2, but Not ERK1, Mediates Acquired and “De novo” Resistance to Imatinib Mesylate: Implication for CML Therapy</a></div><div class="wp-workCard_item"><span>PLoS ONE</span><span>, 2009</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="943c78832b38785d39c7cf04900be2da" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":86444928,"asset_id":79877823,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/86444928/download_file?st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="79877823"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="79877823"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 79877823; 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Most of the studies about resistance have focused on point mutations on BCR/ABL. However, other types of resistance that do not imply mutations in BCR/ABL have been also described. In the present report we aim to study the role of several MAPK in IM resistance not associate to BCR/ABL mutations. Therefore we used an experimental system of resistant cell lines generated by co-culturing with IM (K562, Lama 84) as well as primary material from resistant and responder patient without BCR/ABL mutations. Here we demonstrate that Erk5 and p38MAPK signaling pathways are not implicated in the acquired resistance phenotype. However, Erk2, but not Erk1, is critical for the acquired resistance to IM. In fact, Bcr/Abl activates preferentially Erk2 in transient transfection in a dose dependent fashion through the c-Abl part of the chimeric protein. Finally, we present evidences demonstrating how constitutive activation of Erk2 is a de novo mechanism of resistance to IM. In summary our data support the use of therapeutic approaches based on Erk2 inhibition, which could be added to the therapeutic armamentarium to fight CML, especially when IM resistance develops secondary to Erk2 activation.","publication_date":{"day":null,"month":null,"year":2009,"errors":{}},"publication_name":"PLoS 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class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/79877783/Specific_oncolytic_effect_of_a_new_hypoxia_inducible_factor_dependent_replicative_adenovirus_on_von_Hippel_Lindau_defective_renal_cell_carcinomas">Specific oncolytic effect of a new hypoxia-inducible factor-dependent replicative adenovirus on von Hippel-Lindau-defective renal cell carcinomas</a></div><div class="wp-workCard_item"><span>Cancer research</span><span>, Jan 15, 2003</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Mutations in the von Hippel-Lindau (VHL) tumor suppressor gene are responsible for a hereditary c...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Mutations in the von Hippel-Lindau (VHL) tumor suppressor gene are responsible for a hereditary cancer syndrome characterized by high susceptibility to hemangioblastomas of the retina and central nervous system, pheochromocytomas, and renal cell carcinomas. In agreement with its role as a tumor suppressor, the vast majority of spontaneous clear cell carcinomas of the kidney present loss of heterozygosity at the VHL locus. Recently, it has been shown that VHL works as the substrate recognition component of an E3 ubiquitination complex that targets the hypoxia-inducible factor (HIF) for proteosomal degradation. Under normal oxygen tension, the half-life of HIF transcription factors is extremely short because of its high degradation rate by the proteasome, resulting in undetectable HIF activity in normal cells. However, in VHL-deficient tumor cells, the HIF transcriptional pathway is constitutively activated because of impaired ubiquitination of this transcription factor. To target VHL...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="16c043c1b5de8d1063cf3f1c3fbf3ff1" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":86444885,"asset_id":79877783,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/86444885/download_file?st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="79877783"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="79877783"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 79877783; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=79877783]").text(description); $(".js-view-count[data-work-id=79877783]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 79877783; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='79877783']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 79877783, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "16c043c1b5de8d1063cf3f1c3fbf3ff1" } } $('.js-work-strip[data-work-id=79877783]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":79877783,"title":"Specific oncolytic effect of a new hypoxia-inducible factor-dependent replicative adenovirus on von Hippel-Lindau-defective renal cell carcinomas","translated_title":"","metadata":{"abstract":"Mutations in the von Hippel-Lindau (VHL) tumor suppressor gene are responsible for a hereditary cancer syndrome characterized by high susceptibility to hemangioblastomas of the retina and central nervous system, pheochromocytomas, and renal cell carcinomas. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74437504"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74437504/Hypoxia_inducible_factor_and_cancer"><img alt="Research paper thumbnail of Hypoxia-inducible factor and cancer" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74437504/Hypoxia_inducible_factor_and_cancer">Hypoxia-inducible factor and cancer</a></div><div class="wp-workCard_item"><span>Revista de Oncología</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Oxygen is an essential requirement for mammalian cell metabolism. Cells respond to decreased oxyg...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Oxygen is an essential requirement for mammalian cell metabolism. Cells respond to decreased oxygen tension by inducing adaptive responses aimed at restoring oxygen availability and maintaining energy balance. Most responses to hypoxia are mediated by the activation of a family of transcription factors termed hypoxia-inducible factors (HIF). HIF have been shown to regulate vascular endothelial growth factor (VEGF) produced by</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437504"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437504"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437504; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437504]").text(description); $(".js-view-count[data-work-id=74437504]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437504; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437504']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437504, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=74437504]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437504,"title":"Hypoxia-inducible factor and cancer","translated_title":"","metadata":{"abstract":"Oxygen is an essential requirement for mammalian cell metabolism. 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Ras proteins are molecular switches with the ability to interact and activate several effector molecules. Among those, Raf-1 kinase, PI3K and Ral-GDS are the best characterised. Raf activates the mitogenic MEK/ERK kinases pathway, while PI3K regulates the PKB/Akt cascade, involved in the control of proliferation, metabolism and apoptotic responses. Finally, Ral-GDS belongs to a family of guanine nucleotide exchange factors that activate Ral GTPases. While Raf and PI3K have emerged as critical elements in regulating cell growth and apoptosis, little is known about the role of the Ral-GDS family. We have previously reported that Ras proteins are critical elements in the regulation of phospholipase D (PLD), a proposed target for the Ral-GDS/RalA pathway. Physiological regulation of PLD by growth factors requires the simultaneous activation of ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437502"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437502"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437502; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437502]").text(description); $(".js-view-count[data-work-id=74437502]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437502; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437502']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437502, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=74437502]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437502,"title":"Modulation of phospholipase D by Ras proteins mediated by its effectors Ral-GDS, PI3K and Raf-1","translated_title":"","metadata":{"abstract":"Transformation by ras oncogenes induces the deregulation of intracellular signalling cascades that are critical elements in cell growth control. 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Physiological regulation of PLD by growth factors requires the simultaneous activation of ...","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"publication_name":"International Journal of Oncology"},"translated_abstract":"Transformation by ras oncogenes induces the deregulation of intracellular signalling cascades that are critical elements in cell growth control. Ras proteins are molecular switches with the ability to interact and activate several effector molecules. Among those, Raf-1 kinase, PI3K and Ral-GDS are the best characterised. Raf activates the mitogenic MEK/ERK kinases pathway, while PI3K regulates the PKB/Akt cascade, involved in the control of proliferation, metabolism and apoptotic responses. Finally, Ral-GDS belongs to a family of guanine nucleotide exchange factors that activate Ral GTPases. While Raf and PI3K have emerged as critical elements in regulating cell growth and apoptosis, little is known about the role of the Ral-GDS family. We have previously reported that Ras proteins are critical elements in the regulation of phospholipase D (PLD), a proposed target for the Ral-GDS/RalA pathway. 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Our","internal_url":"https://www.academia.edu/74437501/SOFTWARE_Open_Access_The_Transcription_Factor_Encyclopedia","translated_internal_url":"","created_at":"2022-03-24T00:57:09.978-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":33592395,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":82591590,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82591590/thumbnails/1.jpg","file_name":"gb-2012-13-3-r24.pdf","download_url":"https://www.academia.edu/attachments/82591590/download_file?st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"SOFTWARE_Open_Access_The_Transcription_F.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82591590/gb-2012-13-3-r24-libre.pdf?1648109362=\u0026response-content-disposition=attachment%3B+filename%3DSOFTWARE_Open_Access_The_Transcription_F.pdf\u0026Expires=1733010812\u0026Signature=Rk4kCWc5J~sjZQz1SkjEQvaFC5EHg3oup~70jRNZgcXEcaecyl7jefbOypqka7SkEALcnIPnXjLFGxBr2kWaBeDtOINQ9XsO5qDPepOVknfgn8RChenrcHtE2~Zt8bDrBu4FAlR-U9kbnoh6kvT~AKHpe1p6IqTYX3zNrIHyJVkJrPX-TE6E6Fq8u~YblgGcC2ne2zJUA0XHHHrGxxY3JU9Ibjj2g8~72P~yeGGdV1~UvjkfSibnu~oObLOGOajKGWhrjH9nLOkfogREqiNxv7uEUsKqzCzdJ~duthrUssCqAGsKEK~~sN5RwY5pBCVTEFiYqAldf53zRRhiA~WmiQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"SOFTWARE_Open_Access_The_Transcription_Factor_Encyclopedia","translated_slug":"","page_count":26,"language":"en","content_type":"Work","owner":{"id":33592395,"first_name":"Luis","middle_initials":null,"last_name":"Peso","page_name":"LuisPeso","domain_name":"uam","created_at":"2015-08-04T01:22:11.189-07:00","display_name":"Luis Peso","url":"https://uam.academia.edu/LuisPeso"},"attachments":[{"id":82591590,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82591590/thumbnails/1.jpg","file_name":"gb-2012-13-3-r24.pdf","download_url":"https://www.academia.edu/attachments/82591590/download_file?st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"SOFTWARE_Open_Access_The_Transcription_F.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82591590/gb-2012-13-3-r24-libre.pdf?1648109362=\u0026response-content-disposition=attachment%3B+filename%3DSOFTWARE_Open_Access_The_Transcription_F.pdf\u0026Expires=1733010812\u0026Signature=Rk4kCWc5J~sjZQz1SkjEQvaFC5EHg3oup~70jRNZgcXEcaecyl7jefbOypqka7SkEALcnIPnXjLFGxBr2kWaBeDtOINQ9XsO5qDPepOVknfgn8RChenrcHtE2~Zt8bDrBu4FAlR-U9kbnoh6kvT~AKHpe1p6IqTYX3zNrIHyJVkJrPX-TE6E6Fq8u~YblgGcC2ne2zJUA0XHHHrGxxY3JU9Ibjj2g8~72P~yeGGdV1~UvjkfSibnu~oObLOGOajKGWhrjH9nLOkfogREqiNxv7uEUsKqzCzdJ~duthrUssCqAGsKEK~~sN5RwY5pBCVTEFiYqAldf53zRRhiA~WmiQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[],"urls":[{"id":18753753,"url":"http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.592.8495\u0026rep=rep1\u0026type=pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74437500"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74437500/Formal_meta_analysis_of_hypoxic_gene_expression_profiles_reveals_a_universal_gene_signature_and_cell_type_specific_effects"><img alt="Research paper thumbnail of Formal meta-analysis of hypoxic gene expression profiles reveals a universal gene signature and cell type-specific effects" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74437500/Formal_meta_analysis_of_hypoxic_gene_expression_profiles_reveals_a_universal_gene_signature_and_cell_type_specific_effects">Formal meta-analysis of hypoxic gene expression profiles reveals a universal gene signature and cell type-specific effects</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">BackgroundIntegrating transcriptional profiles results in the identification of gene expression s...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">BackgroundIntegrating transcriptional profiles results in the identification of gene expression signatures that are more robust than those obtained for individual datasets. However, direct comparison of datasets derived from heterogeneous experimental conditions is not possible and their integration requires the application of specific meta-analysis techniques. The transcriptional response to hypoxia has been the focus of intense research due to its central role in tissue homeostasis and in prevalent diseases. Accordingly, a large number of studies have determined the gene expression profile of hypoxic cells. Yet, in spite of this wealth of information, little effort have been done to integrate these dataset to produce a robust hypoxic signature.ResultsWe applied a formal meta-analysis procedure to a dataset comprising 425 RNAseq samples derived from 42 individual studies including 33 different cell types, to derive a pooled estimate of the effect of hypoxia on gene expression. This...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437500"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437500"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437500; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437500]").text(description); $(".js-view-count[data-work-id=74437500]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437500; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437500']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437500, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=74437500]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437500,"title":"Formal meta-analysis of hypoxic gene expression profiles reveals a universal gene signature and cell type-specific effects","translated_title":"","metadata":{"abstract":"BackgroundIntegrating transcriptional profiles results in the identification of gene expression signatures that are more robust than those obtained for individual datasets. However, direct comparison of datasets derived from heterogeneous experimental conditions is not possible and their integration requires the application of specific meta-analysis techniques. The transcriptional response to hypoxia has been the focus of intense research due to its central role in tissue homeostasis and in prevalent diseases. Accordingly, a large number of studies have determined the gene expression profile of hypoxic cells. Yet, in spite of this wealth of information, little effort have been done to integrate these dataset to produce a robust hypoxic signature.ResultsWe applied a formal meta-analysis procedure to a dataset comprising 425 RNAseq samples derived from 42 individual studies including 33 different cell types, to derive a pooled estimate of the effect of hypoxia on gene expression. This...","publisher":"Cold Spring Harbor Laboratory"},"translated_abstract":"BackgroundIntegrating transcriptional profiles results in the identification of gene expression signatures that are more robust than those obtained for individual datasets. However, direct comparison of datasets derived from heterogeneous experimental conditions is not possible and their integration requires the application of specific meta-analysis techniques. The transcriptional response to hypoxia has been the focus of intense research due to its central role in tissue homeostasis and in prevalent diseases. Accordingly, a large number of studies have determined the gene expression profile of hypoxic cells. Yet, in spite of this wealth of information, little effort have been done to integrate these dataset to produce a robust hypoxic signature.ResultsWe applied a formal meta-analysis procedure to a dataset comprising 425 RNAseq samples derived from 42 individual studies including 33 different cell types, to derive a pooled estimate of the effect of hypoxia on gene expression. This...","internal_url":"https://www.academia.edu/74437500/Formal_meta_analysis_of_hypoxic_gene_expression_profiles_reveals_a_universal_gene_signature_and_cell_type_specific_effects","translated_internal_url":"","created_at":"2022-03-24T00:57:09.796-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":33592395,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Formal_meta_analysis_of_hypoxic_gene_expression_profiles_reveals_a_universal_gene_signature_and_cell_type_specific_effects","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":33592395,"first_name":"Luis","middle_initials":null,"last_name":"Peso","page_name":"LuisPeso","domain_name":"uam","created_at":"2015-08-04T01:22:11.189-07:00","display_name":"Luis Peso","url":"https://uam.academia.edu/LuisPeso"},"attachments":[],"research_interests":[],"urls":[{"id":18753752,"url":"https://syndication.highwire.org/content/doi/10.1101/2021.11.12.468418"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74437499"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74437499/Comparative_Study_of_Organoids_from_Patient_Derived_Normal_and_Tumor_Colon_and_Rectal_Tissue"><img alt="Research paper thumbnail of Comparative Study of Organoids from Patient-Derived Normal and Tumor Colon and Rectal Tissue" class="work-thumbnail" src="https://attachments.academia-assets.com/82591543/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74437499/Comparative_Study_of_Organoids_from_Patient_Derived_Normal_and_Tumor_Colon_and_Rectal_Tissue">Comparative Study of Organoids from Patient-Derived Normal and Tumor Colon and Rectal Tissue</a></div><div class="wp-workCard_item"><span>Cancers</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Colon and rectal tumors, often referred to as colorectal cancer, show different gene expression p...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Colon and rectal tumors, often referred to as colorectal cancer, show different gene expression patterns in studies that analyze whole tissue biopsies containing a mix of tumor and non-tumor cells. To better characterize colon and rectal tumors, we investigated the gene expression profile of organoids generated from endoscopic biopsies of rectal tumors and adjacent normal colon and rectum mucosa from therapy-naive rectal cancer patients. We also studied the effect of vitamin D on these organoid types. Gene profiling was performed by RNA-sequencing. Organoids from a normal colon and rectum had a shared gene expression profile that profoundly differed from that of rectal tumor organoids. We identified a group of genes of the biosynthetic machinery as rectal tumor organoid-specific, including those encoding the RNA polymerase II subunits POLR2H and POLR2J. The active vitamin D metabolite 1α,25-dihydroxyvitamin D3/calcitriol upregulated stemness-related genes (LGR5, LRIG1, SMOC2, and MS...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="77c1a7268b39341a999254ec7e41a1f0" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82591543,"asset_id":74437499,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82591543/download_file?st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437499"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437499"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437499; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437499]").text(description); $(".js-view-count[data-work-id=74437499]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437499; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437499']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437499, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "77c1a7268b39341a999254ec7e41a1f0" } } $('.js-work-strip[data-work-id=74437499]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437499,"title":"Comparative Study of Organoids from Patient-Derived Normal and Tumor Colon and Rectal Tissue","translated_title":"","metadata":{"abstract":"Colon and rectal tumors, often referred to as colorectal cancer, show different gene expression patterns in studies that analyze whole tissue biopsies containing a mix of tumor and non-tumor cells. 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However, most transcriptomic studies do not distinguish the relative contribution of transcription, RNA processing and RNA degradation processes to cellular homeostasis. Here we used metabolic labeling followed by massive parallel sequencing of newly transcribed and preexisting RNA fractions to simultaneously analyze RNA synthesis and decay in primary endothelial cells exposed to low oxygen tension. We found that the changes in transcription rates induced by hypoxia are the major determinant of RNA levels. However, degradation rates also had a significant contribution, accounting for 24% of the observed variability in total mRNA. In addition, our results indicated that hypoxia led to a reduction of the overall mRNA stability from a median half-life in normoxia of 8.7 hours, to 5.7 hours in hypoxia. Analysis of RNA content per cell confirmed a dec...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="10c46ff036d6599fe2a338017176771a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82591592,"asset_id":74437498,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82591592/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437498"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437498"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437498; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437498]").text(description); $(".js-view-count[data-work-id=74437498]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437498; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437498']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437498, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "10c46ff036d6599fe2a338017176771a" } } $('.js-work-strip[data-work-id=74437498]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437498,"title":"Metabolic labelling of RNA uncovers the contribution of transcription and decay rates on hypoxia-induced changes in RNA levels","translated_title":"","metadata":{"abstract":"Cells adapt to environmental changes, including fluctuations in oxygen levels, through the induction of specific gene expression programs. 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In addition, our results indicated that hypoxia led to a reduction of the overall mRNA stability from a median half-life in normoxia of 8.7 hours, to 5.7 hours in hypoxia. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74437495"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74437495/Vitamin_D_and_Wnt3A_have_additive_and_partially_overlapping_modulatory_effects_on_gene_expression_and_phenotype_in_human_colon_fibroblasts"><img alt="Research paper thumbnail of Vitamin D and Wnt3A have additive and partially overlapping modulatory effects on gene expression and phenotype in human colon fibroblasts" class="work-thumbnail" src="https://attachments.academia-assets.com/82591547/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74437495/Vitamin_D_and_Wnt3A_have_additive_and_partially_overlapping_modulatory_effects_on_gene_expression_and_phenotype_in_human_colon_fibroblasts">Vitamin D and Wnt3A have additive and partially overlapping modulatory effects on gene expression and phenotype in human colon fibroblasts</a></div><div class="wp-workCard_item"><span>Scientific Reports</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="98e7fcd23f493ced806fd4eae68f4278" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82591547,"asset_id":74437495,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82591547/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437495"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437495"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437495; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "98e7fcd23f493ced806fd4eae68f4278" } } $('.js-work-strip[data-work-id=74437495]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437495,"title":"Vitamin D and Wnt3A have additive and partially overlapping modulatory effects on gene expression and phenotype in human colon fibroblasts","translated_title":"","metadata":{"publisher":"Springer Science and Business Media LLC","grobid_abstract":"The Wnt/β-catenin signalling pathway is essential for intestinal epithelium homeostasis, but its aberrant activation is a hallmark of colorectal cancer (CRC). Several studies indicate that the bioactive vitamin D metabolite 1α,25-dihydroxyvitamin D 3 (1,25(OH) 2 D 3) inhibits proliferation and promotes epithelial differentiation of colon carcinoma cells in part through antagonism of the Wnt/β-catenin pathway. It is now accepted that stromal fibroblasts are crucial in healthy and pathologic intestine: pericryptal myofibroblasts are constituents of the stem cell niche and cancer-associated fibroblasts (CAFs) contribute to CRC progression. However, studies on the combined action of 1,25(OH) 2 D 3 and Wnt factors in colon fibroblasts are lacking. Here we show by global transcriptomic studies that 1,25(OH) 2 D 3 and Wnt3A have profound, additive, partially overlapping effects on the gene expression profile of CCD-18Co human colon myofibroblasts. Moreover, 1,25(OH) 2 D 3 and Wnt3A inhibit CCD-18Co cell proliferation and migration, while 1,25(OH) 2 D 3 reduces, but Wnt3A increases, their capacity to contract collagen gels (a marker of fibroblast activation). These data were largely confirmed in patient-derived primary colon normal fibroblasts and CAFs, and in fibroblasts from other origins. Our results indicate that 1,25(OH) 2 D 3 and Wnt3A are strong regulators of colon fibroblast biology and contribute to a better knowledge of intestinal homeostasis and stromal fibroblast action in CRC. The intestinal epithelium (small intestine and colorectum) is the most intensively renewing adult tissue. It undergoes rapid turnover to prevent the accumulation of DNA damage due to external factors. This process is sustained by stem cells that reside at the bottom of the intestinal crypts and generate proliferative progenitors that subsequently give rise to the specialized differentiated cells. Several signals are required to maintain the homeostasis of intestinal stem cells, among them canonical Wnt factors have a prominent role 1-3. These Wnt proteins are provided by cellular components of the stem cell niche such as Paneth cells (only in the small intestine) and pericryptal myofibroblasts 3-5. Extracellular canonical Wnts bind to their cell membrane receptors and promote an intracellular signalling cascade (known as the Wnt/β-catenin or canonical Wnt signalling pathway) that leads to the translocation of β-catenin to the cell nucleus. There, it binds DNA-bound transcription factors of the T-cell factor (TCF) family and acts as a transcriptional co-activator for several genes that are crucial to preserve the stemness and the undifferentiated phenotype of intestinal stem cells 6. Colorectal cancer (CRC) is a major health problem and one of the leading causes of cancer-related deaths worldwide 7. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74437493"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74437493/Intussusceptive_Vascular_Remodeling_Precedes_Pathological_Neovascularization"><img alt="Research paper thumbnail of Intussusceptive Vascular Remodeling Precedes Pathological Neovascularization" class="work-thumbnail" src="https://attachments.academia-assets.com/82591589/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74437493/Intussusceptive_Vascular_Remodeling_Precedes_Pathological_Neovascularization">Intussusceptive Vascular Remodeling Precedes Pathological Neovascularization</a></div><div class="wp-workCard_item"><span>Arteriosclerosis, Thrombosis, and Vascular Biology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Objective— Pathological neovascularization is crucial for progression and morbidity of serious di...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Objective— Pathological neovascularization is crucial for progression and morbidity of serious diseases such as cancer, diabetic retinopathy, and age-related macular degeneration. While mechanisms of ongoing pathological neovascularization have been extensively studied, the initiating pathological vascular remodeling (PVR) events, which precede neovascularization remains poorly understood. Here, we identify novel molecular and cellular mechanisms of preneovascular PVR, by using the adult choriocapillaris as a model. Approach and Results— Using hypoxia or forced overexpression of VEGF (vascular endothelial growth factor) in the subretinal space to induce PVR in zebrafish and rats respectively, and by analyzing choriocapillaris membranes adjacent to choroidal neovascular lesions from age-related macular degeneration patients, we show that the choriocapillaris undergo robust induction of vascular intussusception and permeability at preneovascular stages of PVR. This PVR response includ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a01d7148b2cd858899fc503f01069f7a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82591589,"asset_id":74437493,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82591589/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437493"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437493"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437493; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437493]").text(description); $(".js-view-count[data-work-id=74437493]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437493; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437493']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437493, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "a01d7148b2cd858899fc503f01069f7a" } } $('.js-work-strip[data-work-id=74437493]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437493,"title":"Intussusceptive Vascular Remodeling Precedes Pathological Neovascularization","translated_title":"","metadata":{"abstract":"Objective— Pathological neovascularization is crucial for progression and morbidity of serious diseases such as cancer, diabetic retinopathy, and age-related macular degeneration. While mechanisms of ongoing pathological neovascularization have been extensively studied, the initiating pathological vascular remodeling (PVR) events, which precede neovascularization remains poorly understood. Here, we identify novel molecular and cellular mechanisms of preneovascular PVR, by using the adult choriocapillaris as a model. Approach and Results— Using hypoxia or forced overexpression of VEGF (vascular endothelial growth factor) in the subretinal space to induce PVR in zebrafish and rats respectively, and by analyzing choriocapillaris membranes adjacent to choroidal neovascular lesions from age-related macular degeneration patients, we show that the choriocapillaris undergo robust induction of vascular intussusception and permeability at preneovascular stages of PVR. This PVR response includ...","publisher":"Ovid Technologies (Wolters Kluwer Health)","publication_name":"Arteriosclerosis, Thrombosis, and Vascular Biology"},"translated_abstract":"Objective— Pathological neovascularization is crucial for progression and morbidity of serious diseases such as cancer, diabetic retinopathy, and age-related macular degeneration. While mechanisms of ongoing pathological neovascularization have been extensively studied, the initiating pathological vascular remodeling (PVR) events, which precede neovascularization remains poorly understood. Here, we identify novel molecular and cellular mechanisms of preneovascular PVR, by using the adult choriocapillaris as a model. Approach and Results— Using hypoxia or forced overexpression of VEGF (vascular endothelial growth factor) in the subretinal space to induce PVR in zebrafish and rats respectively, and by analyzing choriocapillaris membranes adjacent to choroidal neovascular lesions from age-related macular degeneration patients, we show that the choriocapillaris undergo robust induction of vascular intussusception and permeability at preneovascular stages of PVR. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74437490"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74437490/TFEA_ChIP_A_tool_kit_for_transcription_factor_binding_site_enrichment_analysis_capitalizing_on_ChIP_seq_datasets"><img alt="Research paper thumbnail of TFEA.ChIP: A tool kit for transcription factor binding site enrichment analysis capitalizing on ChIP-seq datasets" class="work-thumbnail" src="https://attachments.academia-assets.com/82591587/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74437490/TFEA_ChIP_A_tool_kit_for_transcription_factor_binding_site_enrichment_analysis_capitalizing_on_ChIP_seq_datasets">TFEA.ChIP: A tool kit for transcription factor binding site enrichment analysis capitalizing on ChIP-seq datasets</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The identification of transcription factors (TFs) responsible for the co-regulation of specific s...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The identification of transcription factors (TFs) responsible for the co-regulation of specific sets of genes is a common problem in transcriptomics. Herein we describe TFEA.ChIP, a tool to estimate and visualize TF enrichment in gene lists representing transcriptional profiles. To generate the gene sets representing TF targets, we gathered ChIP-Seq experiments from the ENCODE Consortium and GEO datasets and used the correlation between Dnase Hypersensitive Sites across cell lines to generate a database linking TFs with the genes they interact with in each ChIP-Seq experiment. In its current state, TFEA.ChIP covers 327 different transcription factors from 1075 ChIP-Seq experiments, with over 150 cell types being represented. TFEA.ChIP accepts gene sets as well as sorted lists differentially expressed genes to compute enrichment scores for each of the datasets in its internal database using an Fisher’s exact association test or a Gene Set Enrichment Analysis. We validated TFEA.ChIP u...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="365a717e831d8587838e60a730113405" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82591587,"asset_id":74437490,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82591587/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437490"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437490"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437490; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437490]").text(description); $(".js-view-count[data-work-id=74437490]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437490; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437490']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437490, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "365a717e831d8587838e60a730113405" } } $('.js-work-strip[data-work-id=74437490]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437490,"title":"TFEA.ChIP: A tool kit for transcription factor binding site enrichment analysis capitalizing on ChIP-seq datasets","translated_title":"","metadata":{"abstract":"The identification of transcription factors (TFs) responsible for the co-regulation of specific sets of genes is a common problem in transcriptomics. Herein we describe TFEA.ChIP, a tool to estimate and visualize TF enrichment in gene lists representing transcriptional profiles. To generate the gene sets representing TF targets, we gathered ChIP-Seq experiments from the ENCODE Consortium and GEO datasets and used the correlation between Dnase Hypersensitive Sites across cell lines to generate a database linking TFs with the genes they interact with in each ChIP-Seq experiment. In its current state, TFEA.ChIP covers 327 different transcription factors from 1075 ChIP-Seq experiments, with over 150 cell types being represented. TFEA.ChIP accepts gene sets as well as sorted lists differentially expressed genes to compute enrichment scores for each of the datasets in its internal database using an Fisher’s exact association test or a Gene Set Enrichment Analysis. We validated TFEA.ChIP u...","publisher":"Cold Spring Harbor Laboratory"},"translated_abstract":"The identification of transcription factors (TFs) responsible for the co-regulation of specific sets of genes is a common problem in transcriptomics. Herein we describe TFEA.ChIP, a tool to estimate and visualize TF enrichment in gene lists representing transcriptional profiles. To generate the gene sets representing TF targets, we gathered ChIP-Seq experiments from the ENCODE Consortium and GEO datasets and used the correlation between Dnase Hypersensitive Sites across cell lines to generate a database linking TFs with the genes they interact with in each ChIP-Seq experiment. In its current state, TFEA.ChIP covers 327 different transcription factors from 1075 ChIP-Seq experiments, with over 150 cell types being represented. TFEA.ChIP accepts gene sets as well as sorted lists differentially expressed genes to compute enrichment scores for each of the datasets in its internal database using an Fisher’s exact association test or a Gene Set Enrichment Analysis. We validated TFEA.ChIP u...","internal_url":"https://www.academia.edu/74437490/TFEA_ChIP_A_tool_kit_for_transcription_factor_binding_site_enrichment_analysis_capitalizing_on_ChIP_seq_datasets","translated_internal_url":"","created_at":"2022-03-24T00:57:08.699-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":33592395,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":82591587,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82591587/thumbnails/1.jpg","file_name":"303651.full.pdf","download_url":"https://www.academia.edu/attachments/82591587/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"TFEA_ChIP_A_tool_kit_for_transcription_f.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82591587/303651.full-libre.pdf?1648109359=\u0026response-content-disposition=attachment%3B+filename%3DTFEA_ChIP_A_tool_kit_for_transcription_f.pdf\u0026Expires=1733010813\u0026Signature=O8I2REFjwIyEgphmhQ0DVBmjNij7itx8yQApdfGBRR4oflIRv2ajkr8ceMhQNk6g3i9dE0mhwTuNhujeQFS1ZxotVKrqVBa~f3dr~Tw3z5WpwUYc4m4h1ebvV-k6vAVKQ8lty5INIkVaWl1U4IYLMrXGgBfPSTO9jnbpxlssRRPAoht7eWa-NfWB~cnIFZjmhPZ871RRQvTxDa7HMBsWhQDQPm9-tvESSDMcrLf3jNTTsL0MMNkw6JpNhhFwju8WKQIU7nz0vVuQEVj9nxsjCSraURgiuQqmDuCgjJpGgfhgMOMCJ8l2Wv3hpVKTWg04SWILc0ExttlKw7O28D2LNw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"TFEA_ChIP_A_tool_kit_for_transcription_factor_binding_site_enrichment_analysis_capitalizing_on_ChIP_seq_datasets","translated_slug":"","page_count":11,"language":"en","content_type":"Work","owner":{"id":33592395,"first_name":"Luis","middle_initials":null,"last_name":"Peso","page_name":"LuisPeso","domain_name":"uam","created_at":"2015-08-04T01:22:11.189-07:00","display_name":"Luis Peso","url":"https://uam.academia.edu/LuisPeso"},"attachments":[{"id":82591587,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82591587/thumbnails/1.jpg","file_name":"303651.full.pdf","download_url":"https://www.academia.edu/attachments/82591587/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"TFEA_ChIP_A_tool_kit_for_transcription_f.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82591587/303651.full-libre.pdf?1648109359=\u0026response-content-disposition=attachment%3B+filename%3DTFEA_ChIP_A_tool_kit_for_transcription_f.pdf\u0026Expires=1733010813\u0026Signature=O8I2REFjwIyEgphmhQ0DVBmjNij7itx8yQApdfGBRR4oflIRv2ajkr8ceMhQNk6g3i9dE0mhwTuNhujeQFS1ZxotVKrqVBa~f3dr~Tw3z5WpwUYc4m4h1ebvV-k6vAVKQ8lty5INIkVaWl1U4IYLMrXGgBfPSTO9jnbpxlssRRPAoht7eWa-NfWB~cnIFZjmhPZ871RRQvTxDa7HMBsWhQDQPm9-tvESSDMcrLf3jNTTsL0MMNkw6JpNhhFwju8WKQIU7nz0vVuQEVj9nxsjCSraURgiuQqmDuCgjJpGgfhgMOMCJ8l2Wv3hpVKTWg04SWILc0ExttlKw7O28D2LNw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":146,"name":"Bioinformatics","url":"https://www.academia.edu/Documents/in/Bioinformatics"}],"urls":[{"id":18753744,"url":"https://syndication.highwire.org/content/doi/10.1101/303651"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74437487"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74437487/Hypoxia_and_Chromatin_a_Focus_on_Transcriptional_Repression_Mechanisms"><img alt="Research paper thumbnail of Hypoxia and Chromatin, a Focus on Transcriptional Repression Mechanisms" class="work-thumbnail" src="https://attachments.academia-assets.com/82591584/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74437487/Hypoxia_and_Chromatin_a_Focus_on_Transcriptional_Repression_Mechanisms">Hypoxia and Chromatin, a Focus on Transcriptional Repression Mechanisms</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Hypoxia, or reduced oxygen availability, has been studied extensively for its ability to activate...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Hypoxia, or reduced oxygen availability, has been studied extensively for its ability to activate specific genes. Hypoxia induced gene expression is mediated by the HIF transcription factors, although not exclusively so. Despite the great knowledge on the mechanisms by which hypoxia activates genes, much less is known about how hypoxia promotes gene repression. In this review, we discuss the potential mechanisms underlying hypoxia-induced transcriptional repression responses. We highlight HIF-dependent and independent mechanisms, but also the potential roles of dioxygenases with functions at the nucleosome and DNA level. Finally, we discuss recent evidence regarding the involvement of transcriptional repressor complexes in hypoxia.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="19efaf8d4ec8231923f52657891ff915" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82591584,"asset_id":74437487,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82591584/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437487"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437487"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437487; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437487]").text(description); $(".js-view-count[data-work-id=74437487]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437487; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437487']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437487, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "19efaf8d4ec8231923f52657891ff915" } } $('.js-work-strip[data-work-id=74437487]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437487,"title":"Hypoxia and Chromatin, a Focus on Transcriptional Repression Mechanisms","translated_title":"","metadata":{"abstract":"Hypoxia, or reduced oxygen availability, has been studied extensively for its ability to activate specific genes. Hypoxia induced gene expression is mediated by the HIF transcription factors, although not exclusively so. Despite the great knowledge on the mechanisms by which hypoxia activates genes, much less is known about how hypoxia promotes gene repression. In this review, we discuss the potential mechanisms underlying hypoxia-induced transcriptional repression responses. We highlight HIF-dependent and independent mechanisms, but also the potential roles of dioxygenases with functions at the nucleosome and DNA level. Finally, we discuss recent evidence regarding the involvement of transcriptional repressor complexes in hypoxia.","publisher":"MDPI AG"},"translated_abstract":"Hypoxia, or reduced oxygen availability, has been studied extensively for its ability to activate specific genes. Hypoxia induced gene expression is mediated by the HIF transcription factors, although not exclusively so. Despite the great knowledge on the mechanisms by which hypoxia activates genes, much less is known about how hypoxia promotes gene repression. In this review, we discuss the potential mechanisms underlying hypoxia-induced transcriptional repression responses. We highlight HIF-dependent and independent mechanisms, but also the potential roles of dioxygenases with functions at the nucleosome and DNA level. Finally, we discuss recent evidence regarding the involvement of transcriptional repressor complexes in hypoxia.","internal_url":"https://www.academia.edu/74437487/Hypoxia_and_Chromatin_a_Focus_on_Transcriptional_Repression_Mechanisms","translated_internal_url":"","created_at":"2022-03-24T00:57:08.577-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":33592395,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":82591584,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82591584/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/82591584/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Hypoxia_and_Chromatin_a_Focus_on_Transcr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82591584/pdf-libre.pdf?1648109361=\u0026response-content-disposition=attachment%3B+filename%3DHypoxia_and_Chromatin_a_Focus_on_Transcr.pdf\u0026Expires=1733010813\u0026Signature=Ml7m0sdR0JG6m6ltIxKw4PM53dI4h3iyTDjEsjIX56u1uJ2I7fwSiVO0RYk0wiKwM8kVkg9~pOGTREJm~bYw9rEPeWPIv4oGx1-1UXjfHi5aeKDEL03Al07CrPovywhHlbTDiejDgo60gz0pvs2rpt0n-xUNX9yucMqOEQDlgssoWSD7zKMNUXEllP5~4YGZ19p04Pf0Sz0izH5X237bWurVGG2UAeBm-CCbVx2ajU9tHjd6vnbAvQBo8Jk6kODiOm3T~WoOxgPVqSxm0p2fI9E5tLsdaT9mzRRW6ESVWjco7G-eFrgK233ShD3lGJ4B1wcemfGvXHHF5Y5phe2YmA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Hypoxia_and_Chromatin_a_Focus_on_Transcriptional_Repression_Mechanisms","translated_slug":"","page_count":19,"language":"en","content_type":"Work","owner":{"id":33592395,"first_name":"Luis","middle_initials":null,"last_name":"Peso","page_name":"LuisPeso","domain_name":"uam","created_at":"2015-08-04T01:22:11.189-07:00","display_name":"Luis Peso","url":"https://uam.academia.edu/LuisPeso"},"attachments":[{"id":82591584,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82591584/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/82591584/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Hypoxia_and_Chromatin_a_Focus_on_Transcr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82591584/pdf-libre.pdf?1648109361=\u0026response-content-disposition=attachment%3B+filename%3DHypoxia_and_Chromatin_a_Focus_on_Transcr.pdf\u0026Expires=1733010813\u0026Signature=Ml7m0sdR0JG6m6ltIxKw4PM53dI4h3iyTDjEsjIX56u1uJ2I7fwSiVO0RYk0wiKwM8kVkg9~pOGTREJm~bYw9rEPeWPIv4oGx1-1UXjfHi5aeKDEL03Al07CrPovywhHlbTDiejDgo60gz0pvs2rpt0n-xUNX9yucMqOEQDlgssoWSD7zKMNUXEllP5~4YGZ19p04Pf0Sz0izH5X237bWurVGG2UAeBm-CCbVx2ajU9tHjd6vnbAvQBo8Jk6kODiOm3T~WoOxgPVqSxm0p2fI9E5tLsdaT9mzRRW6ESVWjco7G-eFrgK233ShD3lGJ4B1wcemfGvXHHF5Y5phe2YmA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":1485949,"name":"Preprints","url":"https://www.academia.edu/Documents/in/Preprints"},{"id":3687363,"name":"biomedicines","url":"https://www.academia.edu/Documents/in/biomedicines"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> </div><div class="profile--tab_content_container js-tab-pane tab-pane" data-section-id="3329068" id="papers"><div class="js-work-strip profile--work_container" data-work-id="99959024"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/99959024/Disruption_of_the_CED_9_center_dot_CED_4_complex_by_EGL_1_is_a_critical_step_for_programmed_cell_death_in_Caenorhabditis_elegans"><img alt="Research paper thumbnail of Disruption of the CED-9 center dot CED-4 complex by EGL-1 is a critical step for programmed cell death in Caenorhabditis elegans" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/99959024/Disruption_of_the_CED_9_center_dot_CED_4_complex_by_EGL_1_is_a_critical_step_for_programmed_cell_death_in_Caenorhabditis_elegans">Disruption of the CED-9 center dot CED-4 complex by EGL-1 is a critical step for programmed cell death in Caenorhabditis elegans</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In the nematode Caenorhabditis elegans, the apoptotic machinery is composed of four basic element...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">In the nematode Caenorhabditis elegans, the apoptotic machinery is composed of four basic elements: the caspase CED-3, the Apaf-1 homologue CED-4, and the Bcl-2 family members CED-9 and EGL-1. The ced-9(n1950) gain-of-function mutation prevents most, if not all, somatic cell deaths in C. elegans. It encodes a CED-9 protein with a glycine-to-glutamate substitution at position 169, which is located within the highly conserved Bcl-2 homology 1 domain, We performed biochemical analyses with the CED-9G169E protein to gain insight into the mechanism of programmed cell death, We find that CED-9G169E retains the ability to bind both EGL-1 and CED-4, although its affinity for EGL-1 is reduced. In contrast to the behavior of wild-type CED-9, the interaction between CED-9G169E and CED-4 is not disrupted by expression of EGL-1. Furthermore, CED-4 and CED-9G169E co-localizes with EGL-1 to the mitochondria in mammalian cells, and expression of EGL-1 does not induce translocation of CED-4 to the c...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="99959024"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="99959024"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 99959024; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=99959024]").text(description); $(".js-view-count[data-work-id=99959024]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 99959024; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='99959024']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 99959024, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=99959024]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":99959024,"title":"Disruption of the CED-9 center dot CED-4 complex by EGL-1 is a critical step for programmed cell death in Caenorhabditis elegans","translated_title":"","metadata":{"abstract":"In the nematode Caenorhabditis elegans, the apoptotic machinery is composed of four basic elements: the caspase CED-3, the Apaf-1 homologue CED-4, and the Bcl-2 family members CED-9 and EGL-1. The ced-9(n1950) gain-of-function mutation prevents most, if not all, somatic cell deaths in C. elegans. It encodes a CED-9 protein with a glycine-to-glutamate substitution at position 169, which is located within the highly conserved Bcl-2 homology 1 domain, We performed biochemical analyses with the CED-9G169E protein to gain insight into the mechanism of programmed cell death, We find that CED-9G169E retains the ability to bind both EGL-1 and CED-4, although its affinity for EGL-1 is reduced. In contrast to the behavior of wild-type CED-9, the interaction between CED-9G169E and CED-4 is not disrupted by expression of EGL-1. Furthermore, CED-4 and CED-9G169E co-localizes with EGL-1 to the mitochondria in mammalian cells, and expression of EGL-1 does not induce translocation of CED-4 to the c..."},"translated_abstract":"In the nematode Caenorhabditis elegans, the apoptotic machinery is composed of four basic elements: the caspase CED-3, the Apaf-1 homologue CED-4, and the Bcl-2 family members CED-9 and EGL-1. The ced-9(n1950) gain-of-function mutation prevents most, if not all, somatic cell deaths in C. elegans. It encodes a CED-9 protein with a glycine-to-glutamate substitution at position 169, which is located within the highly conserved Bcl-2 homology 1 domain, We performed biochemical analyses with the CED-9G169E protein to gain insight into the mechanism of programmed cell death, We find that CED-9G169E retains the ability to bind both EGL-1 and CED-4, although its affinity for EGL-1 is reduced. In contrast to the behavior of wild-type CED-9, the interaction between CED-9G169E and CED-4 is not disrupted by expression of EGL-1. Furthermore, CED-4 and CED-9G169E co-localizes with EGL-1 to the mitochondria in mammalian cells, and expression of EGL-1 does not induce translocation of CED-4 to the c...","internal_url":"https://www.academia.edu/99959024/Disruption_of_the_CED_9_center_dot_CED_4_complex_by_EGL_1_is_a_critical_step_for_programmed_cell_death_in_Caenorhabditis_elegans","translated_internal_url":"","created_at":"2023-04-10T00:39:01.466-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":33592395,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Disruption_of_the_CED_9_center_dot_CED_4_complex_by_EGL_1_is_a_critical_step_for_programmed_cell_death_in_Caenorhabditis_elegans","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":33592395,"first_name":"Luis","middle_initials":null,"last_name":"Peso","page_name":"LuisPeso","domain_name":"uam","created_at":"2015-08-04T01:22:11.189-07:00","display_name":"Luis Peso","url":"https://uam.academia.edu/LuisPeso"},"attachments":[],"research_interests":[],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="99959023"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/99959023/MECHANISMS_OF_SIGNAL_TRANSDUCTION_Hypoxia_induces_the_activation_of_the_phosphatidylinositol_3_kinase_Akt_cell_survival_pathway_in_PC12_cells_Protective_role_in_apoptosis"><img alt="Research paper thumbnail of MECHANISMS OF SIGNAL TRANSDUCTION-Hypoxia induces the activation of the phosphatidylinositol 3-kinase/Akt cell survival pathway in PC12 cells. Protective role in apoptosis" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/99959023/MECHANISMS_OF_SIGNAL_TRANSDUCTION_Hypoxia_induces_the_activation_of_the_phosphatidylinositol_3_kinase_Akt_cell_survival_pathway_in_PC12_cells_Protective_role_in_apoptosis">MECHANISMS OF SIGNAL TRANSDUCTION-Hypoxia induces the activation of the phosphatidylinositol 3-kinase/Akt cell survival pathway in PC12 cells. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="99959014"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/99959014/Identification_of_a_region_on_hypoxia_inducible_factor_prolyl_4_hydroxylases_that_determines_their_specificity_for_the_oxygen_degradation_domains"><img alt="Research paper thumbnail of Identification of a region on hypoxia-inducible-factor prolyl 4-hydroxylases that determines their specificity for the oxygen degradation domains" class="work-thumbnail" src="https://attachments.academia-assets.com/100910160/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/99959014/Identification_of_a_region_on_hypoxia_inducible_factor_prolyl_4_hydroxylases_that_determines_their_specificity_for_the_oxygen_degradation_domains">Identification of a region on hypoxia-inducible-factor prolyl 4-hydroxylases that determines their specificity for the oxygen degradation domains</a></div><div class="wp-workCard_item"><span>Biochemical Journal</span><span>, 2007</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">HIFs [hypoxia-inducible (transcription) factors] are essential for the induction of an adaptive g...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">HIFs [hypoxia-inducible (transcription) factors] are essential for the induction of an adaptive gene expression programme under low oxygen partial pressure. The activity of these transcription factors is mainly determined by the stability of the HIFα subunit, which is regulated, in an oxygen-dependent manner, by a family of three prolyl 4-hydroxylases [EGLN1–EGLN3 (EGL nine homologues 1–3)]. HIFα contains two, N- and C-terminal, independent ODDs (oxygen-dependent degradation domains), namely NODD and CODD, that, upon hydroxylation by the EGLNs, target HIFα for proteasomal degradation. In vitro studies indicate that each EGLN shows a differential preference for ODDs, However, the sequence determinants for such specificity are unknown. In the present study we showed that whereas EGLN1 and EGLN2 acted upon any of these ODDs to regulate HIF1α protein levels and activity in vivo, EGLN3 only acted on the CODD. With the aim of identifying the region within EGLNs responsible for their diffe...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9bc0fc55b33e1fa58252f1665353c8e5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":100910160,"asset_id":99959014,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/100910160/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="99959014"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="99959014"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 99959014; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=99959014]").text(description); $(".js-view-count[data-work-id=99959014]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 99959014; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='99959014']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 99959014, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "9bc0fc55b33e1fa58252f1665353c8e5" } } $('.js-work-strip[data-work-id=99959014]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":99959014,"title":"Identification of a region on hypoxia-inducible-factor prolyl 4-hydroxylases that determines their specificity for the oxygen degradation domains","translated_title":"","metadata":{"abstract":"HIFs [hypoxia-inducible (transcription) factors] are essential for the induction of an adaptive gene expression programme under low oxygen partial pressure. The activity of these transcription factors is mainly determined by the stability of the HIFα subunit, which is regulated, in an oxygen-dependent manner, by a family of three prolyl 4-hydroxylases [EGLN1–EGLN3 (EGL nine homologues 1–3)]. HIFα contains two, N- and C-terminal, independent ODDs (oxygen-dependent degradation domains), namely NODD and CODD, that, upon hydroxylation by the EGLNs, target HIFα for proteasomal degradation. In vitro studies indicate that each EGLN shows a differential preference for ODDs, However, the sequence determinants for such specificity are unknown. In the present study we showed that whereas EGLN1 and EGLN2 acted upon any of these ODDs to regulate HIF1α protein levels and activity in vivo, EGLN3 only acted on the CODD. With the aim of identifying the region within EGLNs responsible for their diffe...","publisher":"Portland Press Ltd.","publication_date":{"day":null,"month":null,"year":2007,"errors":{}},"publication_name":"Biochemical Journal"},"translated_abstract":"HIFs [hypoxia-inducible (transcription) factors] are essential for the induction of an adaptive gene expression programme under low oxygen partial pressure. The activity of these transcription factors is mainly determined by the stability of the HIFα subunit, which is regulated, in an oxygen-dependent manner, by a family of three prolyl 4-hydroxylases [EGLN1–EGLN3 (EGL nine homologues 1–3)]. HIFα contains two, N- and C-terminal, independent ODDs (oxygen-dependent degradation domains), namely NODD and CODD, that, upon hydroxylation by the EGLNs, target HIFα for proteasomal degradation. In vitro studies indicate that each EGLN shows a differential preference for ODDs, However, the sequence determinants for such specificity are unknown. In the present study we showed that whereas EGLN1 and EGLN2 acted upon any of these ODDs to regulate HIF1α protein levels and activity in vivo, EGLN3 only acted on the CODD. 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class="js-work-strip profile--work_container" data-work-id="91598449"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/91598449/Nod1_an_Apaf_1_like_Activator_of_Caspase_9_and_Nuclear_Factor_%CE%BAB"><img alt="Research paper thumbnail of Nod1, an Apaf-1-like Activator of Caspase-9 and Nuclear Factor-κB" class="work-thumbnail" src="https://attachments.academia-assets.com/94840992/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/91598449/Nod1_an_Apaf_1_like_Activator_of_Caspase_9_and_Nuclear_Factor_%CE%BAB">Nod1, an Apaf-1-like Activator of Caspase-9 and Nuclear Factor-κB</a></div><div class="wp-workCard_item"><span>Journal of Biological Chemistry</span><span>, 1999</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="15411fbdb892423da8cf3f628f86b30f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":94840992,"asset_id":91598449,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/94840992/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="91598449"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item 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{"id":91598449,"title":"Nod1, an Apaf-1-like Activator of Caspase-9 and Nuclear Factor-κB","translated_title":"","metadata":{"publisher":"Elsevier BV","ai_title_tag":"Nod1: A Novel Apaf-1-like Regulator of Caspase-9 and NF-kB","grobid_abstract":"Ced-4 and Apaf-1 belong to a major class of apoptosis regulators that contain caspase-recruitment (CARD) and nucleotide-binding oligomerization domains. Nod1, a protein with an NH 2-terminal CARD-linked to a nucleotide-binding domain and a COOH-terminal segment with multiple leucine-rich repeats, was identified. Nod-1 was found to bind to multiple caspases with long prodomains, but specifically activated caspase-9 and promoted caspase-9-induced apoptosis. As reported for Apaf-1, Nod1 required both the CARD and P-loop for function. Unlike Apaf-1, Nod1 induced activation of nuclear factor-kappa-B (NF-B) and bound RICK, a CARDcontaining kinase that also induces NF-B activation. Nod1 mutants inhibited NF-B activity induced by RICK, but not that resulting from tumor necrosis factor-␣ stimulation. Thus, Nod1 is a leucine-rich repeatcontaining Apaf-1-like molecule that can regulate both apoptosis and NF-B activation pathways. Apoptosis, or programmed cell death, is a process that is essential for normal development and homeostasis of multicellular organisms (1-3). Genetic studies in the nematode Caenorhabditis elegans have identified core components of the death machinery, which are conserved in vertebrates, including humans (1-3). One of these, Ced-4, is required for developmental cell death in the worm (1, 2). Ced-4 physically interacts with Ced-3 and promotes the proteolytic activation of the immature Ced-3 caspase into enzymatically active subunits (4-7). Apaf-1, a mammalian homologue of Ced-4, has been identified (8). Both Apaf-1 and Ced-4 are composed of an NH 2-terminal caspase recruitment domain (CARD) 1 linked to a nucleotide-binding domain (NBD), also known as the NB-ARC or NOD domain (3, 8-10). Ced-4 and Apaf-1 self-associate via the NBD, a process that mediates proximity and activation of immature Ced-3/caspase-9 molecules (11-13). The COOH-terminal region of Apaf-1 lacks homology with Ced-4 and is composed of 12 WD-40 repeats (8). In response to certain apoptotic stimuli, cytochrome c is released from the mitochondria and binds to Apaf-1 (8, 14), and in the presence of dATP or ATP, Apaf-1 associates with and activates procaspase-9 (8, 14). Recent analyses of Apaf-1-deficient mice suggest a central role of Apaf-1 in apoptosis induced by chemotherapeutic drugs, ultraviolet radiation, and signals associated with neuronal development (15, 16). Mutant mice deficient in caspase-9 exhibit abnormalities similar, but not identical, to those observed in mice lacking Apaf-1 (17, 18). Unlike C. elegans, mice and humans contain multiple initiator caspases, suggesting that mammalian genomes may contain caspase activators other than Apaf-1. Significantly, Apaf-1 knockout mice lack apparent abnormalities in tissues, such as the thymus, whose appropriate cellular development depends on apoptosis (15, 16). The latter observation suggests the existence of additional Apaf-1like molecules or apoptosis pathways that are Apaf-1-independent. In this study, we identified and characterized Nod1, an Apaf-1-like protein that associates with and regulates procaspase-9. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="79877823"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/79877823/ERK2_but_Not_ERK1_Mediates_Acquired_and_De_novo_Resistance_to_Imatinib_Mesylate_Implication_for_CML_Therapy"><img alt="Research paper thumbnail of ERK2, but Not ERK1, Mediates Acquired and “De novo” Resistance to Imatinib Mesylate: Implication for CML Therapy" class="work-thumbnail" src="https://attachments.academia-assets.com/86444928/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/79877823/ERK2_but_Not_ERK1_Mediates_Acquired_and_De_novo_Resistance_to_Imatinib_Mesylate_Implication_for_CML_Therapy">ERK2, but Not ERK1, Mediates Acquired and “De novo” Resistance to Imatinib Mesylate: Implication for CML Therapy</a></div><div class="wp-workCard_item"><span>PLoS ONE</span><span>, 2009</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="943c78832b38785d39c7cf04900be2da" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":86444928,"asset_id":79877823,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/86444928/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="79877823"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="79877823"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 79877823; 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Most of the studies about resistance have focused on point mutations on BCR/ABL. However, other types of resistance that do not imply mutations in BCR/ABL have been also described. In the present report we aim to study the role of several MAPK in IM resistance not associate to BCR/ABL mutations. Therefore we used an experimental system of resistant cell lines generated by co-culturing with IM (K562, Lama 84) as well as primary material from resistant and responder patient without BCR/ABL mutations. Here we demonstrate that Erk5 and p38MAPK signaling pathways are not implicated in the acquired resistance phenotype. However, Erk2, but not Erk1, is critical for the acquired resistance to IM. In fact, Bcr/Abl activates preferentially Erk2 in transient transfection in a dose dependent fashion through the c-Abl part of the chimeric protein. Finally, we present evidences demonstrating how constitutive activation of Erk2 is a de novo mechanism of resistance to IM. In summary our data support the use of therapeutic approaches based on Erk2 inhibition, which could be added to the therapeutic armamentarium to fight CML, especially when IM resistance develops secondary to Erk2 activation.","publication_date":{"day":null,"month":null,"year":2009,"errors":{}},"publication_name":"PLoS 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class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/79877783/Specific_oncolytic_effect_of_a_new_hypoxia_inducible_factor_dependent_replicative_adenovirus_on_von_Hippel_Lindau_defective_renal_cell_carcinomas">Specific oncolytic effect of a new hypoxia-inducible factor-dependent replicative adenovirus on von Hippel-Lindau-defective renal cell carcinomas</a></div><div class="wp-workCard_item"><span>Cancer research</span><span>, Jan 15, 2003</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Mutations in the von Hippel-Lindau (VHL) tumor suppressor gene are responsible for a hereditary c...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Mutations in the von Hippel-Lindau (VHL) tumor suppressor gene are responsible for a hereditary cancer syndrome characterized by high susceptibility to hemangioblastomas of the retina and central nervous system, pheochromocytomas, and renal cell carcinomas. In agreement with its role as a tumor suppressor, the vast majority of spontaneous clear cell carcinomas of the kidney present loss of heterozygosity at the VHL locus. Recently, it has been shown that VHL works as the substrate recognition component of an E3 ubiquitination complex that targets the hypoxia-inducible factor (HIF) for proteosomal degradation. Under normal oxygen tension, the half-life of HIF transcription factors is extremely short because of its high degradation rate by the proteasome, resulting in undetectable HIF activity in normal cells. However, in VHL-deficient tumor cells, the HIF transcriptional pathway is constitutively activated because of impaired ubiquitination of this transcription factor. To target VHL...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="16c043c1b5de8d1063cf3f1c3fbf3ff1" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":86444885,"asset_id":79877783,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/86444885/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="79877783"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="79877783"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 79877783; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=79877783]").text(description); $(".js-view-count[data-work-id=79877783]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 79877783; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='79877783']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 79877783, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "16c043c1b5de8d1063cf3f1c3fbf3ff1" } } $('.js-work-strip[data-work-id=79877783]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":79877783,"title":"Specific oncolytic effect of a new hypoxia-inducible factor-dependent replicative adenovirus on von Hippel-Lindau-defective renal cell carcinomas","translated_title":"","metadata":{"abstract":"Mutations in the von Hippel-Lindau (VHL) tumor suppressor gene are responsible for a hereditary cancer syndrome characterized by high susceptibility to hemangioblastomas of the retina and central nervous system, pheochromocytomas, and renal cell carcinomas. 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To target VHL...","ai_title_tag":"Oncolytic Adenovirus Targeting VHL-Defective Renal Carcinomas","publication_date":{"day":15,"month":1,"year":2003,"errors":{}},"publication_name":"Cancer research"},"translated_abstract":"Mutations in the von Hippel-Lindau (VHL) tumor suppressor gene are responsible for a hereditary cancer syndrome characterized by high susceptibility to hemangioblastomas of the retina and central nervous system, pheochromocytomas, and renal cell carcinomas. In agreement with its role as a tumor suppressor, the vast majority of spontaneous clear cell carcinomas of the kidney present loss of heterozygosity at the VHL locus. Recently, it has been shown that VHL works as the substrate recognition component of an E3 ubiquitination complex that targets the hypoxia-inducible factor (HIF) for proteosomal degradation. Under normal oxygen tension, the half-life of HIF transcription factors is extremely short because of its high degradation rate by the proteasome, resulting in undetectable HIF activity in normal cells. However, in VHL-deficient tumor cells, the HIF transcriptional pathway is constitutively activated because of impaired ubiquitination of this transcription factor. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74437504"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74437504/Hypoxia_inducible_factor_and_cancer"><img alt="Research paper thumbnail of Hypoxia-inducible factor and cancer" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74437504/Hypoxia_inducible_factor_and_cancer">Hypoxia-inducible factor and cancer</a></div><div class="wp-workCard_item"><span>Revista de Oncología</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Oxygen is an essential requirement for mammalian cell metabolism. Cells respond to decreased oxyg...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Oxygen is an essential requirement for mammalian cell metabolism. Cells respond to decreased oxygen tension by inducing adaptive responses aimed at restoring oxygen availability and maintaining energy balance. Most responses to hypoxia are mediated by the activation of a family of transcription factors termed hypoxia-inducible factors (HIF). HIF have been shown to regulate vascular endothelial growth factor (VEGF) produced by</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437504"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437504"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437504; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437504]").text(description); $(".js-view-count[data-work-id=74437504]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437504; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437504']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437504, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=74437504]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437504,"title":"Hypoxia-inducible factor and cancer","translated_title":"","metadata":{"abstract":"Oxygen is an essential requirement for mammalian cell metabolism. 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Ras proteins are molecular switches with the ability to interact and activate several effector molecules. Among those, Raf-1 kinase, PI3K and Ral-GDS are the best characterised. Raf activates the mitogenic MEK/ERK kinases pathway, while PI3K regulates the PKB/Akt cascade, involved in the control of proliferation, metabolism and apoptotic responses. Finally, Ral-GDS belongs to a family of guanine nucleotide exchange factors that activate Ral GTPases. While Raf and PI3K have emerged as critical elements in regulating cell growth and apoptosis, little is known about the role of the Ral-GDS family. We have previously reported that Ras proteins are critical elements in the regulation of phospholipase D (PLD), a proposed target for the Ral-GDS/RalA pathway. Physiological regulation of PLD by growth factors requires the simultaneous activation of ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437502"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437502"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437502; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437502]").text(description); $(".js-view-count[data-work-id=74437502]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437502; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437502']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437502, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=74437502]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437502,"title":"Modulation of phospholipase D by Ras proteins mediated by its effectors Ral-GDS, PI3K and Raf-1","translated_title":"","metadata":{"abstract":"Transformation by ras oncogenes induces the deregulation of intracellular signalling cascades that are critical elements in cell growth control. 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Physiological regulation of PLD by growth factors requires the simultaneous activation of ...","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"publication_name":"International Journal of Oncology"},"translated_abstract":"Transformation by ras oncogenes induces the deregulation of intracellular signalling cascades that are critical elements in cell growth control. Ras proteins are molecular switches with the ability to interact and activate several effector molecules. Among those, Raf-1 kinase, PI3K and Ral-GDS are the best characterised. Raf activates the mitogenic MEK/ERK kinases pathway, while PI3K regulates the PKB/Akt cascade, involved in the control of proliferation, metabolism and apoptotic responses. Finally, Ral-GDS belongs to a family of guanine nucleotide exchange factors that activate Ral GTPases. While Raf and PI3K have emerged as critical elements in regulating cell growth and apoptosis, little is known about the role of the Ral-GDS family. We have previously reported that Ras proteins are critical elements in the regulation of phospholipase D (PLD), a proposed target for the Ral-GDS/RalA pathway. Physiological regulation of PLD by growth factors requires the simultaneous activation of ...","internal_url":"https://www.academia.edu/74437502/Modulation_of_phospholipase_D_by_Ras_proteins_mediated_by_its_effectors_Ral_GDS_PI3K_and_Raf_1","translated_internal_url":"","created_at":"2022-03-24T00:57:10.175-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":33592395,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Modulation_of_phospholipase_D_by_Ras_proteins_mediated_by_its_effectors_Ral_GDS_PI3K_and_Raf_1","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":33592395,"first_name":"Luis","middle_initials":null,"last_name":"Peso","page_name":"LuisPeso","domain_name":"uam","created_at":"2015-08-04T01:22:11.189-07:00","display_name":"Luis Peso","url":"https://uam.academia.edu/LuisPeso"},"attachments":[],"research_interests":[{"id":626,"name":"Oncology","url":"https://www.academia.edu/Documents/in/Oncology"},{"id":5072,"name":"Molecular Medicine","url":"https://www.academia.edu/Documents/in/Molecular_Medicine"},{"id":6021,"name":"Cancer","url":"https://www.academia.edu/Documents/in/Cancer"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":9113,"name":"Cell Cycle","url":"https://www.academia.edu/Documents/in/Cell_Cycle"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":74780,"name":"Mutation","url":"https://www.academia.edu/Documents/in/Mutation"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":107533,"name":"Cell","url":"https://www.academia.edu/Documents/in/Cell"},{"id":175647,"name":"T cells","url":"https://www.academia.edu/Documents/in/T_cells"},{"id":181936,"name":"Gene","url":"https://www.academia.edu/Documents/in/Gene"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":620070,"name":"Transfection","url":"https://www.academia.edu/Documents/in/Transfection"},{"id":708643,"name":"Phospholipase D","url":"https://www.academia.edu/Documents/in/Phospholipase_D"},{"id":954995,"name":"Human Fibroblasts","url":"https://www.academia.edu/Documents/in/Human_Fibroblasts"},{"id":2533047,"name":"fibroblasts","url":"https://www.academia.edu/Documents/in/fibroblasts"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74437501"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74437501/SOFTWARE_Open_Access_The_Transcription_Factor_Encyclopedia"><img alt="Research paper thumbnail of SOFTWARE Open Access The Transcription Factor Encyclopedia" class="work-thumbnail" src="https://attachments.academia-assets.com/82591590/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74437501/SOFTWARE_Open_Access_The_Transcription_Factor_Encyclopedia">SOFTWARE Open Access The Transcription Factor Encyclopedia</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Here we present the Transcription Factor Encyclopedia (TFe), a new web-based compendium of mini r...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Here we present the Transcription Factor Encyclopedia (TFe), a new web-based compendium of mini review articles on transcription factors (TFs) that is founded on the principles of open access and collaboration. Our</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="24692d884ed610400e53ec8736bbd6f4" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82591590,"asset_id":74437501,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82591590/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437501"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437501"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437501; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437501]").text(description); $(".js-view-count[data-work-id=74437501]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437501; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437501']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437501, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "24692d884ed610400e53ec8736bbd6f4" } } $('.js-work-strip[data-work-id=74437501]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437501,"title":"SOFTWARE Open Access The Transcription Factor Encyclopedia","translated_title":"","metadata":{"abstract":"Here we present the Transcription Factor Encyclopedia (TFe), a new web-based compendium of mini review articles on transcription factors (TFs) that is founded on the principles of open access and collaboration. 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However, direct comparison of datasets derived from heterogeneous experimental conditions is not possible and their integration requires the application of specific meta-analysis techniques. The transcriptional response to hypoxia has been the focus of intense research due to its central role in tissue homeostasis and in prevalent diseases. Accordingly, a large number of studies have determined the gene expression profile of hypoxic cells. Yet, in spite of this wealth of information, little effort have been done to integrate these dataset to produce a robust hypoxic signature.ResultsWe applied a formal meta-analysis procedure to a dataset comprising 425 RNAseq samples derived from 42 individual studies including 33 different cell types, to derive a pooled estimate of the effect of hypoxia on gene expression. This...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437500"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437500"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437500; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437500]").text(description); $(".js-view-count[data-work-id=74437500]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437500; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437500']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437500, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=74437500]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437500,"title":"Formal meta-analysis of hypoxic gene expression profiles reveals a universal gene signature and cell type-specific effects","translated_title":"","metadata":{"abstract":"BackgroundIntegrating transcriptional profiles results in the identification of gene expression signatures that are more robust than those obtained for individual datasets. 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This...","internal_url":"https://www.academia.edu/74437500/Formal_meta_analysis_of_hypoxic_gene_expression_profiles_reveals_a_universal_gene_signature_and_cell_type_specific_effects","translated_internal_url":"","created_at":"2022-03-24T00:57:09.796-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":33592395,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Formal_meta_analysis_of_hypoxic_gene_expression_profiles_reveals_a_universal_gene_signature_and_cell_type_specific_effects","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":33592395,"first_name":"Luis","middle_initials":null,"last_name":"Peso","page_name":"LuisPeso","domain_name":"uam","created_at":"2015-08-04T01:22:11.189-07:00","display_name":"Luis Peso","url":"https://uam.academia.edu/LuisPeso"},"attachments":[],"research_interests":[],"urls":[{"id":18753752,"url":"https://syndication.highwire.org/content/doi/10.1101/2021.11.12.468418"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74437499"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74437499/Comparative_Study_of_Organoids_from_Patient_Derived_Normal_and_Tumor_Colon_and_Rectal_Tissue"><img alt="Research paper thumbnail of Comparative Study of Organoids from Patient-Derived Normal and Tumor Colon and Rectal Tissue" class="work-thumbnail" src="https://attachments.academia-assets.com/82591543/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74437499/Comparative_Study_of_Organoids_from_Patient_Derived_Normal_and_Tumor_Colon_and_Rectal_Tissue">Comparative Study of Organoids from Patient-Derived Normal and Tumor Colon and Rectal Tissue</a></div><div class="wp-workCard_item"><span>Cancers</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Colon and rectal tumors, often referred to as colorectal cancer, show different gene expression p...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Colon and rectal tumors, often referred to as colorectal cancer, show different gene expression patterns in studies that analyze whole tissue biopsies containing a mix of tumor and non-tumor cells. To better characterize colon and rectal tumors, we investigated the gene expression profile of organoids generated from endoscopic biopsies of rectal tumors and adjacent normal colon and rectum mucosa from therapy-naive rectal cancer patients. We also studied the effect of vitamin D on these organoid types. Gene profiling was performed by RNA-sequencing. Organoids from a normal colon and rectum had a shared gene expression profile that profoundly differed from that of rectal tumor organoids. We identified a group of genes of the biosynthetic machinery as rectal tumor organoid-specific, including those encoding the RNA polymerase II subunits POLR2H and POLR2J. The active vitamin D metabolite 1α,25-dihydroxyvitamin D3/calcitriol upregulated stemness-related genes (LGR5, LRIG1, SMOC2, and MS...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="77c1a7268b39341a999254ec7e41a1f0" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82591543,"asset_id":74437499,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82591543/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437499"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437499"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437499; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437499]").text(description); $(".js-view-count[data-work-id=74437499]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437499; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437499']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437499, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "77c1a7268b39341a999254ec7e41a1f0" } } $('.js-work-strip[data-work-id=74437499]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437499,"title":"Comparative Study of Organoids from Patient-Derived Normal and Tumor Colon and Rectal Tissue","translated_title":"","metadata":{"abstract":"Colon and rectal tumors, often referred to as colorectal cancer, show different gene expression patterns in studies that analyze whole tissue biopsies containing a mix of tumor and non-tumor cells. 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The active vitamin D metabolite 1α,25-dihydroxyvitamin D3/calcitriol upregulated stemness-related genes (LGR5, LRIG1, SMOC2, and MS...","publisher":"MDPI AG","publication_name":"Cancers"},"translated_abstract":"Colon and rectal tumors, often referred to as colorectal cancer, show different gene expression patterns in studies that analyze whole tissue biopsies containing a mix of tumor and non-tumor cells. To better characterize colon and rectal tumors, we investigated the gene expression profile of organoids generated from endoscopic biopsies of rectal tumors and adjacent normal colon and rectum mucosa from therapy-naive rectal cancer patients. We also studied the effect of vitamin D on these organoid types. Gene profiling was performed by RNA-sequencing. Organoids from a normal colon and rectum had a shared gene expression profile that profoundly differed from that of rectal tumor organoids. We identified a group of genes of the biosynthetic machinery as rectal tumor organoid-specific, including those encoding the RNA polymerase II subunits POLR2H and POLR2J. 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However, most transcriptomic studies do not distinguish the relative contribution of transcription, RNA processing and RNA degradation processes to cellular homeostasis. Here we used metabolic labeling followed by massive parallel sequencing of newly transcribed and preexisting RNA fractions to simultaneously analyze RNA synthesis and decay in primary endothelial cells exposed to low oxygen tension. We found that the changes in transcription rates induced by hypoxia are the major determinant of RNA levels. However, degradation rates also had a significant contribution, accounting for 24% of the observed variability in total mRNA. In addition, our results indicated that hypoxia led to a reduction of the overall mRNA stability from a median half-life in normoxia of 8.7 hours, to 5.7 hours in hypoxia. Analysis of RNA content per cell confirmed a dec...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="10c46ff036d6599fe2a338017176771a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82591592,"asset_id":74437498,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82591592/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437498"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437498"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437498; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437498]").text(description); $(".js-view-count[data-work-id=74437498]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437498; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437498']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437498, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "10c46ff036d6599fe2a338017176771a" } } $('.js-work-strip[data-work-id=74437498]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437498,"title":"Metabolic labelling of RNA uncovers the contribution of transcription and decay rates on hypoxia-induced changes in RNA levels","translated_title":"","metadata":{"abstract":"Cells adapt to environmental changes, including fluctuations in oxygen levels, through the induction of specific gene expression programs. However, most transcriptomic studies do not distinguish the relative contribution of transcription, RNA processing and RNA degradation processes to cellular homeostasis. Here we used metabolic labeling followed by massive parallel sequencing of newly transcribed and preexisting RNA fractions to simultaneously analyze RNA synthesis and decay in primary endothelial cells exposed to low oxygen tension. We found that the changes in transcription rates induced by hypoxia are the major determinant of RNA levels. However, degradation rates also had a significant contribution, accounting for 24% of the observed variability in total mRNA. In addition, our results indicated that hypoxia led to a reduction of the overall mRNA stability from a median half-life in normoxia of 8.7 hours, to 5.7 hours in hypoxia. Analysis of RNA content per cell confirmed a dec...","publisher":"Cold Spring Harbor Laboratory"},"translated_abstract":"Cells adapt to environmental changes, including fluctuations in oxygen levels, through the induction of specific gene expression programs. However, most transcriptomic studies do not distinguish the relative contribution of transcription, RNA processing and RNA degradation processes to cellular homeostasis. Here we used metabolic labeling followed by massive parallel sequencing of newly transcribed and preexisting RNA fractions to simultaneously analyze RNA synthesis and decay in primary endothelial cells exposed to low oxygen tension. We found that the changes in transcription rates induced by hypoxia are the major determinant of RNA levels. However, degradation rates also had a significant contribution, accounting for 24% of the observed variability in total mRNA. In addition, our results indicated that hypoxia led to a reduction of the overall mRNA stability from a median half-life in normoxia of 8.7 hours, to 5.7 hours in hypoxia. Analysis of RNA content per cell confirmed a dec...","internal_url":"https://www.academia.edu/74437498/Metabolic_labelling_of_RNA_uncovers_the_contribution_of_transcription_and_decay_rates_on_hypoxia_induced_changes_in_RNA_levels","translated_internal_url":"","created_at":"2022-03-24T00:57:09.434-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":33592395,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":82591592,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82591592/thumbnails/1.jpg","file_name":"694570.full.pdf","download_url":"https://www.academia.edu/attachments/82591592/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Metabolic_labelling_of_RNA_uncovers_the.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82591592/694570.full-libre.pdf?1648109370=\u0026response-content-disposition=attachment%3B+filename%3DMetabolic_labelling_of_RNA_uncovers_the.pdf\u0026Expires=1733010812\u0026Signature=FykOQ2SdtQPUJiWL0Z6NHoHhOCwNKfl2~3nXZB8nu-6IxFfT1IdvEU-GmL-907TzdtfwOBOLZvxVuzvMAlaVR9ThGxjut~VggmPaOSEVpfMiSfj3hRLSkuukJgONhbZUzS3~IXanJEh-hG84HgOaLHgOsBI~RTEsphRcjG2ifAFJO0XKwBfkX2dzoHL9rusGF7F2xZ0SUg4CSOuK00gT8j6b2ORxGwoM9mPGxko7ynUlTlFNUcrFLfMhe~oXmlfWByQ1cac4fBkIjk5HkLupD8oYNEJB271lN6PWMy4ZOew4YIpT8qhOv0a5SIIfxcAP~StYaNv9QJ8Mb4YLTHpYyQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Metabolic_labelling_of_RNA_uncovers_the_contribution_of_transcription_and_decay_rates_on_hypoxia_induced_changes_in_RNA_levels","translated_slug":"","page_count":41,"language":"en","content_type":"Work","owner":{"id":33592395,"first_name":"Luis","middle_initials":null,"last_name":"Peso","page_name":"LuisPeso","domain_name":"uam","created_at":"2015-08-04T01:22:11.189-07:00","display_name":"Luis Peso","url":"https://uam.academia.edu/LuisPeso"},"attachments":[{"id":82591592,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82591592/thumbnails/1.jpg","file_name":"694570.full.pdf","download_url":"https://www.academia.edu/attachments/82591592/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Metabolic_labelling_of_RNA_uncovers_the.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82591592/694570.full-libre.pdf?1648109370=\u0026response-content-disposition=attachment%3B+filename%3DMetabolic_labelling_of_RNA_uncovers_the.pdf\u0026Expires=1733010812\u0026Signature=FykOQ2SdtQPUJiWL0Z6NHoHhOCwNKfl2~3nXZB8nu-6IxFfT1IdvEU-GmL-907TzdtfwOBOLZvxVuzvMAlaVR9ThGxjut~VggmPaOSEVpfMiSfj3hRLSkuukJgONhbZUzS3~IXanJEh-hG84HgOaLHgOsBI~RTEsphRcjG2ifAFJO0XKwBfkX2dzoHL9rusGF7F2xZ0SUg4CSOuK00gT8j6b2ORxGwoM9mPGxko7ynUlTlFNUcrFLfMhe~oXmlfWByQ1cac4fBkIjk5HkLupD8oYNEJB271lN6PWMy4ZOew4YIpT8qhOv0a5SIIfxcAP~StYaNv9QJ8Mb4YLTHpYyQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":3701,"name":"RNA","url":"https://www.academia.edu/Documents/in/RNA"},{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"}],"urls":[{"id":18753750,"url":"https://syndication.highwire.org/content/doi/10.1101/694570"}]}, dispatcherData: dispatcherData }); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74437495"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74437495/Vitamin_D_and_Wnt3A_have_additive_and_partially_overlapping_modulatory_effects_on_gene_expression_and_phenotype_in_human_colon_fibroblasts"><img alt="Research paper thumbnail of Vitamin D and Wnt3A have additive and partially overlapping modulatory effects on gene expression and phenotype in human colon fibroblasts" class="work-thumbnail" src="https://attachments.academia-assets.com/82591547/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74437495/Vitamin_D_and_Wnt3A_have_additive_and_partially_overlapping_modulatory_effects_on_gene_expression_and_phenotype_in_human_colon_fibroblasts">Vitamin D and Wnt3A have additive and partially overlapping modulatory effects on gene expression and phenotype in human colon fibroblasts</a></div><div class="wp-workCard_item"><span>Scientific Reports</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="98e7fcd23f493ced806fd4eae68f4278" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82591547,"asset_id":74437495,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82591547/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437495"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437495"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437495; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "98e7fcd23f493ced806fd4eae68f4278" } } $('.js-work-strip[data-work-id=74437495]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437495,"title":"Vitamin D and Wnt3A have additive and partially overlapping modulatory effects on gene expression and phenotype in human colon fibroblasts","translated_title":"","metadata":{"publisher":"Springer Science and Business Media LLC","grobid_abstract":"The Wnt/β-catenin signalling pathway is essential for intestinal epithelium homeostasis, but its aberrant activation is a hallmark of colorectal cancer (CRC). Several studies indicate that the bioactive vitamin D metabolite 1α,25-dihydroxyvitamin D 3 (1,25(OH) 2 D 3) inhibits proliferation and promotes epithelial differentiation of colon carcinoma cells in part through antagonism of the Wnt/β-catenin pathway. It is now accepted that stromal fibroblasts are crucial in healthy and pathologic intestine: pericryptal myofibroblasts are constituents of the stem cell niche and cancer-associated fibroblasts (CAFs) contribute to CRC progression. However, studies on the combined action of 1,25(OH) 2 D 3 and Wnt factors in colon fibroblasts are lacking. Here we show by global transcriptomic studies that 1,25(OH) 2 D 3 and Wnt3A have profound, additive, partially overlapping effects on the gene expression profile of CCD-18Co human colon myofibroblasts. Moreover, 1,25(OH) 2 D 3 and Wnt3A inhibit CCD-18Co cell proliferation and migration, while 1,25(OH) 2 D 3 reduces, but Wnt3A increases, their capacity to contract collagen gels (a marker of fibroblast activation). These data were largely confirmed in patient-derived primary colon normal fibroblasts and CAFs, and in fibroblasts from other origins. Our results indicate that 1,25(OH) 2 D 3 and Wnt3A are strong regulators of colon fibroblast biology and contribute to a better knowledge of intestinal homeostasis and stromal fibroblast action in CRC. The intestinal epithelium (small intestine and colorectum) is the most intensively renewing adult tissue. It undergoes rapid turnover to prevent the accumulation of DNA damage due to external factors. This process is sustained by stem cells that reside at the bottom of the intestinal crypts and generate proliferative progenitors that subsequently give rise to the specialized differentiated cells. Several signals are required to maintain the homeostasis of intestinal stem cells, among them canonical Wnt factors have a prominent role 1-3. These Wnt proteins are provided by cellular components of the stem cell niche such as Paneth cells (only in the small intestine) and pericryptal myofibroblasts 3-5. Extracellular canonical Wnts bind to their cell membrane receptors and promote an intracellular signalling cascade (known as the Wnt/β-catenin or canonical Wnt signalling pathway) that leads to the translocation of β-catenin to the cell nucleus. There, it binds DNA-bound transcription factors of the T-cell factor (TCF) family and acts as a transcriptional co-activator for several genes that are crucial to preserve the stemness and the undifferentiated phenotype of intestinal stem cells 6. Colorectal cancer (CRC) is a major health problem and one of the leading causes of cancer-related deaths worldwide 7. The initial event in most CRCs is the aberrant activation of the Wnt/β-catenin signalling pathway","publication_name":"Scientific Reports","grobid_abstract_attachment_id":82591547},"translated_abstract":null,"internal_url":"https://www.academia.edu/74437495/Vitamin_D_and_Wnt3A_have_additive_and_partially_overlapping_modulatory_effects_on_gene_expression_and_phenotype_in_human_colon_fibroblasts","translated_internal_url":"","created_at":"2022-03-24T00:57:08.977-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":33592395,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":82591547,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82591547/thumbnails/1.jpg","file_name":"s41598-019-44574-9.pdf","download_url":"https://www.academia.edu/attachments/82591547/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Vitamin_D_and_Wnt3A_have_additive_and_pa.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82591547/s41598-019-44574-9-libre.pdf?1648109364=\u0026response-content-disposition=attachment%3B+filename%3DVitamin_D_and_Wnt3A_have_additive_and_pa.pdf\u0026Expires=1733010813\u0026Signature=gmslW6d1g-6Mg~0ZWL80MH6gx7jq2Ec0trkR4oA9kE6OC3hXy6wBbx6OAtmRKrlupn2b7iwJVugXAH0ystogK7iVazZ3pb3fIDyX-tzcquVhtYuu61U9JJLsJhNhDdEeHknzQwvcbDmuFlErM4MFcOK3FXNArLQuM5OkznCpahj1AFiEQesv2Rrb7p8nyz3yxDhDE3zEZ6tqD84Dg3UiqJvijRifRtLxvkAQSPkuh8VEYUtYI6M1kSxOzgAIISfRIAkqiXL5ZAVGAUh6qO8frcVo7Fs6iIo4vn2KnOBaimdpnltEvj0Xzb9PirNgIvlUw~w-GdOG7xtCZdtANHjBHw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Vitamin_D_and_Wnt3A_have_additive_and_partially_overlapping_modulatory_effects_on_gene_expression_and_phenotype_in_human_colon_fibroblasts","translated_slug":"","page_count":13,"language":"en","content_type":"Work","owner":{"id":33592395,"first_name":"Luis","middle_initials":null,"last_name":"Peso","page_name":"LuisPeso","domain_name":"uam","created_at":"2015-08-04T01:22:11.189-07:00","display_name":"Luis Peso","url":"https://uam.academia.edu/LuisPeso"},"attachments":[{"id":82591547,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82591547/thumbnails/1.jpg","file_name":"s41598-019-44574-9.pdf","download_url":"https://www.academia.edu/attachments/82591547/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Vitamin_D_and_Wnt3A_have_additive_and_pa.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82591547/s41598-019-44574-9-libre.pdf?1648109364=\u0026response-content-disposition=attachment%3B+filename%3DVitamin_D_and_Wnt3A_have_additive_and_pa.pdf\u0026Expires=1733010813\u0026Signature=gmslW6d1g-6Mg~0ZWL80MH6gx7jq2Ec0trkR4oA9kE6OC3hXy6wBbx6OAtmRKrlupn2b7iwJVugXAH0ystogK7iVazZ3pb3fIDyX-tzcquVhtYuu61U9JJLsJhNhDdEeHknzQwvcbDmuFlErM4MFcOK3FXNArLQuM5OkznCpahj1AFiEQesv2Rrb7p8nyz3yxDhDE3zEZ6tqD84Dg3UiqJvijRifRtLxvkAQSPkuh8VEYUtYI6M1kSxOzgAIISfRIAkqiXL5ZAVGAUh6qO8frcVo7Fs6iIo4vn2KnOBaimdpnltEvj0Xzb9PirNgIvlUw~w-GdOG7xtCZdtANHjBHw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":82591548,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82591548/thumbnails/1.jpg","file_name":"s41598-019-44574-9.pdf","download_url":"https://www.academia.edu/attachments/82591548/download_file","bulk_download_file_name":"Vitamin_D_and_Wnt3A_have_additive_and_pa.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82591548/s41598-019-44574-9-libre.pdf?1648109364=\u0026response-content-disposition=attachment%3B+filename%3DVitamin_D_and_Wnt3A_have_additive_and_pa.pdf\u0026Expires=1733010813\u0026Signature=S1efe1pY07w0U4yZRs0HAvCZfxEX1P8MbsbV5ZShWNuNJPs3xygDKwJjbAXB9qh71AomckKdV-gHVtLZEJHJaC559IZnKbsuJ8DKkmo3n~N7qJO9hUn0GKrTDuS1KQ2O7pKjGemfdTnSiOlomtOXptEh7xYeRrPR9pNbnQIs8-olL7cE6y6c7bSfEC0eGJImXVCR4KemhQw2BUMd9iL3EL-la930wDvEJF16mdBB3K5PY175BYoNotu-Xw5AibezYjWpzjGj0aAyNwrCcmDQi~KWe6tAPX0QFK61wTuOZiIe7l3iUujF-nn3hvH2e~2KnpWWepTsYOGrhuhP-3ZpYg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[],"urls":[{"id":18753747,"url":"http://www.nature.com/articles/s41598-019-44574-9.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74437493"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74437493/Intussusceptive_Vascular_Remodeling_Precedes_Pathological_Neovascularization"><img alt="Research paper thumbnail of Intussusceptive Vascular Remodeling Precedes Pathological Neovascularization" class="work-thumbnail" src="https://attachments.academia-assets.com/82591589/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74437493/Intussusceptive_Vascular_Remodeling_Precedes_Pathological_Neovascularization">Intussusceptive Vascular Remodeling Precedes Pathological Neovascularization</a></div><div class="wp-workCard_item"><span>Arteriosclerosis, Thrombosis, and Vascular Biology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Objective— Pathological neovascularization is crucial for progression and morbidity of serious di...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Objective— Pathological neovascularization is crucial for progression and morbidity of serious diseases such as cancer, diabetic retinopathy, and age-related macular degeneration. While mechanisms of ongoing pathological neovascularization have been extensively studied, the initiating pathological vascular remodeling (PVR) events, which precede neovascularization remains poorly understood. Here, we identify novel molecular and cellular mechanisms of preneovascular PVR, by using the adult choriocapillaris as a model. Approach and Results— Using hypoxia or forced overexpression of VEGF (vascular endothelial growth factor) in the subretinal space to induce PVR in zebrafish and rats respectively, and by analyzing choriocapillaris membranes adjacent to choroidal neovascular lesions from age-related macular degeneration patients, we show that the choriocapillaris undergo robust induction of vascular intussusception and permeability at preneovascular stages of PVR. This PVR response includ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a01d7148b2cd858899fc503f01069f7a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82591589,"asset_id":74437493,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82591589/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437493"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437493"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437493; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437493]").text(description); $(".js-view-count[data-work-id=74437493]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437493; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437493']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437493, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "a01d7148b2cd858899fc503f01069f7a" } } $('.js-work-strip[data-work-id=74437493]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437493,"title":"Intussusceptive Vascular Remodeling Precedes Pathological Neovascularization","translated_title":"","metadata":{"abstract":"Objective— Pathological neovascularization is crucial for progression and morbidity of serious diseases such as cancer, diabetic retinopathy, and age-related macular degeneration. While mechanisms of ongoing pathological neovascularization have been extensively studied, the initiating pathological vascular remodeling (PVR) events, which precede neovascularization remains poorly understood. Here, we identify novel molecular and cellular mechanisms of preneovascular PVR, by using the adult choriocapillaris as a model. Approach and Results— Using hypoxia or forced overexpression of VEGF (vascular endothelial growth factor) in the subretinal space to induce PVR in zebrafish and rats respectively, and by analyzing choriocapillaris membranes adjacent to choroidal neovascular lesions from age-related macular degeneration patients, we show that the choriocapillaris undergo robust induction of vascular intussusception and permeability at preneovascular stages of PVR. This PVR response includ...","publisher":"Ovid Technologies (Wolters Kluwer Health)","publication_name":"Arteriosclerosis, Thrombosis, and Vascular Biology"},"translated_abstract":"Objective— Pathological neovascularization is crucial for progression and morbidity of serious diseases such as cancer, diabetic retinopathy, and age-related macular degeneration. While mechanisms of ongoing pathological neovascularization have been extensively studied, the initiating pathological vascular remodeling (PVR) events, which precede neovascularization remains poorly understood. Here, we identify novel molecular and cellular mechanisms of preneovascular PVR, by using the adult choriocapillaris as a model. Approach and Results— Using hypoxia or forced overexpression of VEGF (vascular endothelial growth factor) in the subretinal space to induce PVR in zebrafish and rats respectively, and by analyzing choriocapillaris membranes adjacent to choroidal neovascular lesions from age-related macular degeneration patients, we show that the choriocapillaris undergo robust induction of vascular intussusception and permeability at preneovascular stages of PVR. This PVR response includ...","internal_url":"https://www.academia.edu/74437493/Intussusceptive_Vascular_Remodeling_Precedes_Pathological_Neovascularization","translated_internal_url":"","created_at":"2022-03-24T00:57:08.868-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":33592395,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":82591589,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82591589/thumbnails/1.jpg","file_name":"Intussusceptive_Vascular_Remodeling_Precedes_Pathological_Neovascularization.pdf","download_url":"https://www.academia.edu/attachments/82591589/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Intussusceptive_Vascular_Remodeling_Prec.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82591589/Intussusceptive_Vascular_Remodeling_Precedes_Pathological_Neovascularization-libre.pdf?1648109357=\u0026response-content-disposition=attachment%3B+filename%3DIntussusceptive_Vascular_Remodeling_Prec.pdf\u0026Expires=1733010813\u0026Signature=dX0SL3DQul93wwDxEDhac3SLT2pZR57rK3GCfE6roXZLH0VJY6WrwEExNjZkFLntWd-iCdbeu5pHRyHz8Vv97ycCKVLtMdb8b3T~0N1aIQAVMhjtRiKVOmyi6m9e-~CvtyIweORn~roIeSoeDpXkuSScixEfBxlqky0DRCIs~8IKUotBE6F9B7yCM9PbBAgR9Sq~nynyIpE0T4K~tk1oPN9I2Bn00MMyAquUuc7jHCnZ12rWw6QwzisYlPVrrlDmLuK6gK-9CoNekO~vCjvCwgmMCZg6B08C9igvF~XYzgm36qrJ4JqUER9l8JAc5n0d-koh7NnuRVCt~a4qbJ6S-A__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Intussusceptive_Vascular_Remodeling_Precedes_Pathological_Neovascularization","translated_slug":"","page_count":18,"language":"en","content_type":"Work","owner":{"id":33592395,"first_name":"Luis","middle_initials":null,"last_name":"Peso","page_name":"LuisPeso","domain_name":"uam","created_at":"2015-08-04T01:22:11.189-07:00","display_name":"Luis Peso","url":"https://uam.academia.edu/LuisPeso"},"attachments":[{"id":82591589,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/82591589/thumbnails/1.jpg","file_name":"Intussusceptive_Vascular_Remodeling_Precedes_Pathological_Neovascularization.pdf","download_url":"https://www.academia.edu/attachments/82591589/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Intussusceptive_Vascular_Remodeling_Prec.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/82591589/Intussusceptive_Vascular_Remodeling_Precedes_Pathological_Neovascularization-libre.pdf?1648109357=\u0026response-content-disposition=attachment%3B+filename%3DIntussusceptive_Vascular_Remodeling_Prec.pdf\u0026Expires=1733010813\u0026Signature=dX0SL3DQul93wwDxEDhac3SLT2pZR57rK3GCfE6roXZLH0VJY6WrwEExNjZkFLntWd-iCdbeu5pHRyHz8Vv97ycCKVLtMdb8b3T~0N1aIQAVMhjtRiKVOmyi6m9e-~CvtyIweORn~roIeSoeDpXkuSScixEfBxlqky0DRCIs~8IKUotBE6F9B7yCM9PbBAgR9Sq~nynyIpE0T4K~tk1oPN9I2Bn00MMyAquUuc7jHCnZ12rWw6QwzisYlPVrrlDmLuK6gK-9CoNekO~vCjvCwgmMCZg6B08C9igvF~XYzgm36qrJ4JqUER9l8JAc5n0d-koh7NnuRVCt~a4qbJ6S-A__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":3789879,"name":"Cardiovascular medicine and haematology","url":"https://www.academia.edu/Documents/in/Cardiovascular_medicine_and_haematology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="74437490"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/74437490/TFEA_ChIP_A_tool_kit_for_transcription_factor_binding_site_enrichment_analysis_capitalizing_on_ChIP_seq_datasets"><img alt="Research paper thumbnail of TFEA.ChIP: A tool kit for transcription factor binding site enrichment analysis capitalizing on ChIP-seq datasets" class="work-thumbnail" src="https://attachments.academia-assets.com/82591587/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/74437490/TFEA_ChIP_A_tool_kit_for_transcription_factor_binding_site_enrichment_analysis_capitalizing_on_ChIP_seq_datasets">TFEA.ChIP: A tool kit for transcription factor binding site enrichment analysis capitalizing on ChIP-seq datasets</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The identification of transcription factors (TFs) responsible for the co-regulation of specific s...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The identification of transcription factors (TFs) responsible for the co-regulation of specific sets of genes is a common problem in transcriptomics. Herein we describe TFEA.ChIP, a tool to estimate and visualize TF enrichment in gene lists representing transcriptional profiles. To generate the gene sets representing TF targets, we gathered ChIP-Seq experiments from the ENCODE Consortium and GEO datasets and used the correlation between Dnase Hypersensitive Sites across cell lines to generate a database linking TFs with the genes they interact with in each ChIP-Seq experiment. In its current state, TFEA.ChIP covers 327 different transcription factors from 1075 ChIP-Seq experiments, with over 150 cell types being represented. TFEA.ChIP accepts gene sets as well as sorted lists differentially expressed genes to compute enrichment scores for each of the datasets in its internal database using an Fisher’s exact association test or a Gene Set Enrichment Analysis. We validated TFEA.ChIP u...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="365a717e831d8587838e60a730113405" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":82591587,"asset_id":74437490,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/82591587/download_file?st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&st=MTczMzAwNzIxMyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="74437490"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="74437490"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 74437490; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=74437490]").text(description); $(".js-view-count[data-work-id=74437490]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 74437490; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='74437490']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 74437490, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "365a717e831d8587838e60a730113405" } } $('.js-work-strip[data-work-id=74437490]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":74437490,"title":"TFEA.ChIP: A tool kit for transcription factor binding site enrichment analysis capitalizing on ChIP-seq datasets","translated_title":"","metadata":{"abstract":"The identification of transcription factors (TFs) responsible for the co-regulation of specific sets of genes is a common problem in transcriptomics. Herein we describe TFEA.ChIP, a tool to estimate and visualize TF enrichment in gene lists representing transcriptional profiles. To generate the gene sets representing TF targets, we gathered ChIP-Seq experiments from the ENCODE Consortium and GEO datasets and used the correlation between Dnase Hypersensitive Sites across cell lines to generate a database linking TFs with the genes they interact with in each ChIP-Seq experiment. In its current state, TFEA.ChIP covers 327 different transcription factors from 1075 ChIP-Seq experiments, with over 150 cell types being represented. TFEA.ChIP accepts gene sets as well as sorted lists differentially expressed genes to compute enrichment scores for each of the datasets in its internal database using an Fisher’s exact association test or a Gene Set Enrichment Analysis. We validated TFEA.ChIP u...","publisher":"Cold Spring Harbor Laboratory"},"translated_abstract":"The identification of transcription factors (TFs) responsible for the co-regulation of specific sets of genes is a common problem in transcriptomics. Herein we describe TFEA.ChIP, a tool to estimate and visualize TF enrichment in gene lists representing transcriptional profiles. To generate the gene sets representing TF targets, we gathered ChIP-Seq experiments from the ENCODE Consortium and GEO datasets and used the correlation between Dnase Hypersensitive Sites across cell lines to generate a database linking TFs with the genes they interact with in each ChIP-Seq experiment. In its current state, TFEA.ChIP covers 327 different transcription factors from 1075 ChIP-Seq experiments, with over 150 cell types being represented. TFEA.ChIP accepts gene sets as well as sorted lists differentially expressed genes to compute enrichment scores for each of the datasets in its internal database using an Fisher’s exact association test or a Gene Set Enrichment Analysis. 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Hypoxia induced gene expression is mediated by the HIF transcription factors, although not exclusively so. Despite the great knowledge on the mechanisms by which hypoxia activates genes, much less is known about how hypoxia promotes gene repression. In this review, we discuss the potential mechanisms underlying hypoxia-induced transcriptional repression responses. We highlight HIF-dependent and independent mechanisms, but also the potential roles of dioxygenases with functions at the nucleosome and DNA level. 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