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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 Phillippa Taberlay</h3></div><div class="js-work-strip profile--work_container" data-work-id="69295950"><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/69295950/H3K4me3_enrichment_defines_neuronal_age_while_a_youthful_H3K27ac_signature_is_recapitulated_in_aged_neurons"><img alt="Research paper thumbnail of H3K4me3 enrichment defines neuronal age, while a youthful H3K27ac signature is recapitulated in aged neurons" 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/69295950/H3K4me3_enrichment_defines_neuronal_age_while_a_youthful_H3K27ac_signature_is_recapitulated_in_aged_neurons">H3K4me3 enrichment defines neuronal age, while a youthful H3K27ac signature is recapitulated in aged neurons</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ABSTRACTNeurons live for the lifespan of the individual and underlie our ability for lifelong lea...</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">ABSTRACTNeurons live for the lifespan of the individual and underlie our ability for lifelong learning and memory. However, aging alters neuron morphology and function resulting in age-related cognitive decline. It is well established that epigenetic alterations are essential for learning and memory, yet few neuron-specific genome-wide epigenetic maps exist into old age. Comprehensive mapping of H3K4me3 and H3K27ac in mouse neurons across lifespan revealed plastic H3K4me3 marking that differentiates neuronal age linked to known characteristics of cellular and neuronal aging. We determined that neurons in old age recapitulate the H3K27ac enrichment at promoters, enhancers and super enhancers from young adult neurons, likely representing a re-activation of pathways to maintain neuronal output. Finally, this study identified new characteristics of neuronal aging, including altered rDNA regulation and epigenetic regulatory mechanisms. Collectively, these findings indicate a key role for...</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="69295950"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="69295950"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 69295950; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=69295950]").text(description); $(".js-view-count[data-work-id=69295950]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 69295950; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='69295950']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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" } } $('.js-work-strip[data-work-id=69295950]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":69295950,"title":"H3K4me3 enrichment defines neuronal age, while a youthful H3K27ac signature is recapitulated in aged neurons","internal_url":"https://www.academia.edu/69295950/H3K4me3_enrichment_defines_neuronal_age_while_a_youthful_H3K27ac_signature_is_recapitulated_in_aged_neurons","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[]}, 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="58914884"><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/58914884/DNA_Methylation_and_Cancer"><img alt="Research paper thumbnail of DNA Methylation and Cancer" class="work-thumbnail" src="https://attachments.academia-assets.com/73094115/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/58914884/DNA_Methylation_and_Cancer">DNA Methylation and Cancer</a></div><div class="wp-workCard_item"><span>Journal of Clinical Oncology</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">DNA methylation acts in concert with other epigenetic mechanisms to regulate normal gene expressi...</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">DNA methylation acts in concert with other epigenetic mechanisms to regulate normal gene expression and facilitate chromatin organization within cells. Aberrant DNA methylation patterns are acquired during carcinogenic transformation; such events are often accompanied by alterations in chromatin structure at gene regulatory regions. The expression pattern of any given gene is achieved by interacting epigenetic mechanisms. First, the insertion of nucleosomes at transcriptional start sites prevents the binding of the transcriptional machinery and additional cofactors that initiate gene expression. Second, nucleosomes anchor all of the DNMT3A and DNMT3B methyltransferase proteins in the cell, which suggests a role for histone octamers in the establishment of DNA methylation patterns. During carcinogenesis, epigenetic switching and 5-methylcytosine reprogramming result in the aberrant hypermethylation of CpG islands, reducing epigenetic plasticity of critical developmental and tumor suppressor genes, rendering them unresponsive to normal stimuli. Here, we will discuss the importance of both established and novel molecular concepts that may underlie the role of DNA methylation in cancer.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b11a34ed857e2e629c92cab8014534da" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":73094115,"asset_id":58914884,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/73094115/download_file?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="58914884"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="58914884"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 58914884; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="52927064"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/52927064/Targeting_histone_acetylation_dynamics_and_oncogenic_transcription_by_catalytic_P300_CBP_inhibition"><img alt="Research paper thumbnail of Targeting histone acetylation dynamics and oncogenic transcription by catalytic P300/CBP inhibition" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/52927064/Targeting_histone_acetylation_dynamics_and_oncogenic_transcription_by_catalytic_P300_CBP_inhibition">Targeting histone acetylation dynamics and oncogenic transcription by catalytic P300/CBP inhibition</a></div><div class="wp-workCard_item"><span>Molecular Cell</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="52927064"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927064"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927064; 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</script> <div class="js-work-strip profile--work_container" data-work-id="52927063"><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/52927063/BRG1_knockdown_inhibits_proliferation_through_multiple_cellular_pathways_in_prostate_cancer"><img alt="Research paper thumbnail of BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer" class="work-thumbnail" src="https://attachments.academia-assets.com/69953008/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/52927063/BRG1_knockdown_inhibits_proliferation_through_multiple_cellular_pathways_in_prostate_cancer">BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer</a></div><div class="wp-workCard_item"><span>Clinical Epigenetics</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background BRG1 (encoded by SMARCA4) is a catalytic component of the SWI/SNF chromatin remodellin...</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">Background BRG1 (encoded by SMARCA4) is a catalytic component of the SWI/SNF chromatin remodelling complex, with key roles in modulating DNA accessibility. Dysregulation of BRG1 is observed, but functionally uncharacterised, in a wide range of malignancies. We have probed the functions of BRG1 on a background of prostate cancer to investigate how BRG1 controls gene expression programmes and cancer cell behaviour. Results Our investigation of SMARCA4 revealed that BRG1 is over-expressed in the majority of the 486 tumours from The Cancer Genome Atlas prostate cohort, as well as in a complementary panel of 21 prostate cell lines. Next, we utilised a temporal model of BRG1 depletion to investigate the molecular effects on global transcription programmes. Depleting BRG1 had no impact on alternative splicing and conferred only modest effect on global expression. However, of the transcriptional changes that occurred, most manifested as down-regulated expression. Deeper examination found th...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bec56653b7d3ffaf2b0cc5c3a465ab7f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953008,"asset_id":52927063,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953008/download_file?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="52927063"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927063"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927063; 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$(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="52927062"><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/52927062/BRG1_promotes_transcriptional_patterns_that_are_permissive_to_proliferation_in_cancer_cells"><img alt="Research paper thumbnail of BRG1 promotes transcriptional patterns that are permissive to proliferation in cancer cells" 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/52927062/BRG1_promotes_transcriptional_patterns_that_are_permissive_to_proliferation_in_cancer_cells">BRG1 promotes transcriptional patterns that are permissive to proliferation in cancer cells</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ABSTRACTBackgroundBRG1 (encoded bySMARCA4) is a catalytic component of the SWI/SNF chromatin remo...</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">ABSTRACTBackgroundBRG1 (encoded bySMARCA4) is a catalytic component of the SWI/SNF chromatin remodelling complex, with key roles in modulating DNA accessibility. Dysregulation of BRG1 is observed, but functionally uncharacterised, in a wide range of malignancies. We have probed the functions of BRG1 on a background of prostate cancer to investigate how BRG1 controls gene expression programs and cancer cell behaviour.ResultsOur investigation ofSMARCA4revealed that BRG1 is universally overexpressed in 486 tumours from The Cancer Genome Atlas prostate cohort, as well as in a complementary panel of 21 prostate cell lines. Next, we utilised a temporal model of BRG1 depletion to investigate the molecular effects on global transcription programs. Unexpectedly, depleting BRG1 had no impact on alternative splicing and conferred only modest effect on global expression. However, of the transcriptional changes that occurred, most manifested as down-regulated expression. Deeper examination found...</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="52927062"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927062"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927062; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927062]").text(description); $(".js-view-count[data-work-id=52927062]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927062; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927062']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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" } } $('.js-work-strip[data-work-id=52927062]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":52927062,"title":"BRG1 promotes transcriptional patterns that are permissive to proliferation in cancer cells","internal_url":"https://www.academia.edu/52927062/BRG1_promotes_transcriptional_patterns_that_are_permissive_to_proliferation_in_cancer_cells","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[]}, 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="52927061"><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/52927061/The_DNA_methylation_landscape_in_cancer"><img alt="Research paper thumbnail of The DNA methylation landscape in cancer" class="work-thumbnail" src="https://attachments.academia-assets.com/69953012/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/52927061/The_DNA_methylation_landscape_in_cancer">The DNA methylation landscape in cancer</a></div><div class="wp-workCard_item"><span>Essays in Biochemistry</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">As one of the most abundant and well-studied epigenetic modifications, DNA methylation plays an e...</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">As one of the most abundant and well-studied epigenetic modifications, DNA methylation plays an essential role in normal development and cellular biology. Global alterations to the DNA methylation landscape contribute to alterations in the transcriptome and deregulation of cellular pathways. Indeed, improved methods to study DNA methylation patterning and dynamics at base pair resolution and across individual DNA molecules on a genome-wide scale has highlighted the scope of change to the DNA methylation landscape in disease states, particularly during tumorigenesis. More recently has been the development of DNA hydroxymethylation profiling techniques, which allows differentiation between 5mC and 5hmC profiles and provides further insights into DNA methylation dynamics and remodeling in tumorigenesis. In this review, we describe the distribution of DNA methylation and DNA hydroxymethylation in different genomic contexts, first in normal cells, and how this is altered in cancer. Final...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="863591c750fe19b11c881f6de8a8c2d3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953012,"asset_id":52927061,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953012/download_file?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="52927061"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927061"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927061; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927061]").text(description); $(".js-view-count[data-work-id=52927061]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927061; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927061']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(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="52927060"><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/52927060/Constitutively_bound_CTCF_sites_maintain_3D_chromatin_architecture_and_long_range_epigenetically_regulated_domains"><img alt="Research paper thumbnail of Constitutively bound CTCF sites maintain 3D chromatin architecture and long-range epigenetically regulated domains" class="work-thumbnail" src="https://attachments.academia-assets.com/69953015/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/52927060/Constitutively_bound_CTCF_sites_maintain_3D_chromatin_architecture_and_long_range_epigenetically_regulated_domains">Constitutively bound CTCF sites maintain 3D chromatin architecture and long-range epigenetically regulated domains</a></div><div class="wp-workCard_item"><span>Nature Communications</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The architectural protein CTCF is a mediator of chromatin conformation, but how CTCF binding to D...</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 architectural protein CTCF is a mediator of chromatin conformation, but how CTCF binding to DNA is orchestrated to maintain long-range gene expression is poorly understood. Here we perform RNAi knockdown to reduce CTCF levels and reveal a shared subset of CTCF-bound sites are robustly resistant to protein depletion. The ‘persistent’ CTCF sites are enriched at domain boundaries and chromatin loops constitutive to all cell types. CRISPR-Cas9 deletion of 2 persistent CTCF sites at the boundary between a long-range epigenetically active (LREA) and silenced (LRES) region, within the Kallikrein (KLK) locus, results in concordant activation of all 8 KLK genes within the LRES region. CTCF genome-wide depletion results in alteration in Topologically Associating Domain (TAD) structure, including the merging of TADs, whereas TAD boundaries are not altered where persistent sites are maintained. We propose that the subset of essential CTCF sites are involved in cell-type constitutive, higher...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="87c42288c15366176f58facfbd1c3f8b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953015,"asset_id":52927060,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953015/download_file?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="52927060"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927060"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927060; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927060]").text(description); $(".js-view-count[data-work-id=52927060]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927060; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927060']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(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="52927059"><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/52927059/Xmas_ESC_A_new_female_embryonic_stem_cell_system_that_reveals_the_BAF_complex_as_a_key_regulator_of_the_establishment_of_X_chromosome_inactivation"><img alt="Research paper thumbnail of Xmas ESC: A new female embryonic stem cell system that reveals the BAF complex as a key regulator of the establishment of X chromosome inactivation" class="work-thumbnail" src="https://attachments.academia-assets.com/69953056/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/52927059/Xmas_ESC_A_new_female_embryonic_stem_cell_system_that_reveals_the_BAF_complex_as_a_key_regulator_of_the_establishment_of_X_chromosome_inactivation">Xmas ESC: A new female embryonic stem cell system that reveals the BAF complex as a key regulator of the establishment of X chromosome inactivation</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Although female pluripotency significantly differs to male, complications with in vitro culture o...</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">Although female pluripotency significantly differs to male, complications with in vitro culture of female embryonic stem cells (ESC) have severely limited the use and study of these cells. We report a replenishable female ESC system, Xmas, that has enabled us to optimise a protocol for preserving the XX karyotype. Our protocol also improves male ESC fitness. We utilised our Xmas ESC system to screen for regulators of the female-specific process of X chromosome inactivation, revealing chromatin remodellers Smarcc1 and Smarca4 as key regulators of establishment of X inactivation. The remodellers create a nucleosome depleted region at gene promotors on the inactive X during exit from pluripotency, without which gene silencing fails. Our female ESC system provides a tractable model for XX ESC culture that will expedite study of female pluripotency and has enabled us to discover new features of the female-specific process of X inactivation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="e68ecdf959371ce9638ce92dd8a61268" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953056,"asset_id":52927059,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953056/download_file?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="52927059"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927059"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927059; 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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="52927058"><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/52927058/DNA_methylation_changes_following_DNA_damage_in_prostate_cancer_cells"><img alt="Research paper thumbnail of DNA methylation changes following DNA damage in prostate cancer cells" class="work-thumbnail" src="https://attachments.academia-assets.com/69953007/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/52927058/DNA_methylation_changes_following_DNA_damage_in_prostate_cancer_cells">DNA methylation changes following DNA damage in prostate cancer cells</a></div><div class="wp-workCard_item"><span>Epigenetics</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Many cancer therapies operate by inducing double-strand breaks (DSBs) in cancer cells, however tr...</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">Many cancer therapies operate by inducing double-strand breaks (DSBs) in cancer cells, however treatment-resistant cells rapidly initiate mechanisms to repair damage enabling survival. While the DNA repair mechanisms responsible for cancer cell survival following DNA damaging treatments are becoming better understood, less is known about the role of the epigenome in this process. Using prostate cancer cell lines with differing sensitivities to radiation treatment, we analysed the DNA methylation profiles prior to and following a single dose of radiotherapy (RT) using the Illumina Infinium HumanMethylation450 BeadChip platform. DSB formation and repair, in the absence and presence of the DNA hypomethylating agent, 5-azacytidine (5-AzaC), were also investigated using γH2A.X immunofluorescence staining. Here we demonstrate that DNA methylation is generally stable following a single dose of RT; however, a small number of CpG sites are stably altered up to 14 d following exposure. While the radioresistant and radiosensitive cells displayed distinct basal DNA methylation profiles, their susceptibility to DNA damage appeared similar demonstrating that basal DNA methylation has a limited influence on DSB induction at the regions examined. Recovery from DSB induction was also similar between these cells. Treatment with 5-AzaC did not sensitize resistant cells to DNA damage, but rather delayed recruitment of phosphorylated BRCA1 (S1423) and repair of DSBs. These results highlight that stable epigenetic changes are possible following a single dose of RT and may have significant clinical implications for cancer treatment involving recurrent or fractionated dosing regimens.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="8ea5c009eeb592153983d230e417d719" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953007,"asset_id":52927058,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953007/download_file?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="52927058"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927058"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927058; 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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="52927057"><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/52927057/Age_but_Not_Amyloidosis_Induced_Changes_in_Global_Levels_of_Histone_Modifications_in_Susceptible_and_Disease_Resistant_Neurons_in_Alzheimer_s_Disease_Model_Mice"><img alt="Research paper thumbnail of Age, but Not Amyloidosis, Induced Changes in Global Levels of Histone Modifications in Susceptible and Disease-Resistant Neurons in Alzheimer’s Disease Model Mice" class="work-thumbnail" src="https://attachments.academia-assets.com/69953057/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/52927057/Age_but_Not_Amyloidosis_Induced_Changes_in_Global_Levels_of_Histone_Modifications_in_Susceptible_and_Disease_Resistant_Neurons_in_Alzheimer_s_Disease_Model_Mice">Age, but Not Amyloidosis, Induced Changes in Global Levels of Histone Modifications in Susceptible and Disease-Resistant Neurons in Alzheimer’s Disease Model Mice</a></div><div class="wp-workCard_item"><span>Frontiers in Aging Neuroscience</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">There is increasing interest in the role of epigenetic alterations in Alzheimer's disease (AD). T...</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">There is increasing interest in the role of epigenetic alterations in Alzheimer's disease (AD). The epigenome of every cell type is distinct, yet data regarding epigenetic change in specific cell types in aging and AD is limited. We investigated histone tail modifications in neuronal subtypes in wild-type and APP/PS1 mice at 3 (prepathology), 6 (pathology-onset) and 12 (pathology-rich) months of age. In neurofilament (NF)-positive pyramidal neurons (vulnerable to AD pathology), and in calretinin-labeled interneurons (resistant to AD pathology) there were no global alterations in histone 3 lysine 4 trimethylation (H3K4me3), histone 3 lysine 27 acetylation (H3K27ac) or histone 3 lysine 27 trimethylation (H3K27me3) in APP/PS1 compared to wild-type mice at any age. Interestingly, age-related changes in the presence of H3K27ac and H3K27me3 were detected in NF-labeled pyramidal neurons and calretinin-positive interneurons, respectively. These data suggest that the global levels of histone modifications change with age, whilst amyloid plaque deposition and its sequelae do not result in global alterations of H3K4me3, H3K27ac and H3K27me3 in NF-positive pyramidal neurons or calretinin-labeled interneurons.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="856b6d583adda0816f024e25bb4d1f15" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953057,"asset_id":52927057,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953057/download_file?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="52927057"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927057"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927057; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927057]").text(description); $(".js-view-count[data-work-id=52927057]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927057; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927057']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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: "856b6d583adda0816f024e25bb4d1f15" } } $('.js-work-strip[data-work-id=52927057]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":52927057,"title":"Age, but Not Amyloidosis, Induced Changes in Global Levels of Histone Modifications in Susceptible and Disease-Resistant Neurons in Alzheimer’s Disease Model Mice","internal_url":"https://www.academia.edu/52927057/Age_but_Not_Amyloidosis_Induced_Changes_in_Global_Levels_of_Histone_Modifications_in_Susceptible_and_Disease_Resistant_Neurons_in_Alzheimer_s_Disease_Model_Mice","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[{"id":69953057,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/69953057/thumbnails/1.jpg","file_name":"133062_20-_20Age__20but_20not_20amyloidosis__20induced_20changes_20in_20global_20levels_20of_20histone.pdf","download_url":"https://www.academia.edu/attachments/69953057/download_file","bulk_download_file_name":"Age_but_Not_Amyloidosis_Induced_Changes.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/69953057/133062_20-_20Age__20but_20not_20amyloidosis__20induced_20changes_20in_20global_20levels_20of_20histone-libre.pdf?1632116629=\u0026response-content-disposition=attachment%3B+filename%3DAge_but_Not_Amyloidosis_Induced_Changes.pdf\u0026Expires=1740014889\u0026Signature=Igf1Prj-ScV34Rw9C3OlmcQDOKtdvYYWwwlHJMhCo5PF1DU-5~RCnOCW9zRX6UdCRAu--tkFTBdPSZQhUoTdv7Kwcpl2kQo8cSXrP-927vFze22xr2~3T~UjQI0opJ0I6YXyjk0I5HtZ4bpOJ4iGmZJ--MAlObl95U9~vXG~02yFh5J5H3SvEjd5l32yyNon0ut9RLTZV0DTZyqmGNzy~D6YPAwVx99TJPlZatvI0S15sFSH4y18wJapnfGubitJA8PQVnC-KOKzSkyJA39tPF1hUXzg9shI~8P~BT1u78iwA9MaU6ZCNnsGQuTaWLU1cojlXEsVwuK3VTCLZw0vew__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, 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="52927056"><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/52927056/Integrated_epigenomic_analysis_stratifies_chromatin_remodellers_into_distinct_functional_groups"><img alt="Research paper thumbnail of Integrated epigenomic analysis stratifies chromatin remodellers into distinct functional groups" class="work-thumbnail" src="https://attachments.academia-assets.com/69953004/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/52927056/Integrated_epigenomic_analysis_stratifies_chromatin_remodellers_into_distinct_functional_groups">Integrated epigenomic analysis stratifies chromatin remodellers into distinct functional groups</a></div><div class="wp-workCard_item"><span>Epigenetics & Chromatin</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background: ATP-dependent chromatin remodelling complexes are responsible for establishing and ma...</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">Background: ATP-dependent chromatin remodelling complexes are responsible for establishing and maintaining the positions of nucleosomes. Chromatin remodellers are targeted to chromatin by transcription factors and noncoding RNA to remodel the chromatin into functional states. However, the influence of chromatin remodelling on shaping the functional epigenome is not well understood. Moreover, chromatin remodellers have not been extensively explored as a collective group across two-dimensional and three-dimensional epigenomic layers. Results: Here, we have integrated the genome-wide binding profiles of eight chromatin remodellers together with DNA methylation, nucleosome positioning, histone modification and Hi-C chromosomal contacts to reveal that chromatin remodellers can be stratified into two functional groups. Group 1 (BRG1, SNF2H, CHD3 and CHD4) has a clear preference for binding at 'actively marked' chromatin and Group 2 (BRM, INO80, SNF2L and CHD1) for 'repressively marked' chromatin. We find that histone modifications and chromatin architectural features, but not DNA methylation, stratify the remodellers into these functional groups. Conclusions: Our findings suggest that chromatin remodelling events are synchronous and that chromatin remodellers themselves should be considered simultaneously and not as individual entities in isolation or necessarily by structural similarity, as they are traditionally classified. Their coordinated function should be considered by preference for chromatin features in order to gain a more accurate and comprehensive picture of chromatin regulation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="41c2306ff8249ba5c5d37c1d2369cc52" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953004,"asset_id":52927056,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953004/download_file?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="52927056"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927056"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927056; 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To enable accurate gene regulation, enhancer elements and promoter regions are brought into close spatial proximity to ensure proper, cell type-specific gene expression. In cancer, genetic and epigenetic processes can deregulate the transcriptional program. To investigate whether the 3D chromatin state is also disrupted in cancer we performed Hi-C chromosome conformation sequencing in normal and prostate cancer cells and compared the chromatin interaction maps with changes to the genome and epigenome. Notably, we find that additional topologically associated domain (TAD) boundaries are formed in cancer cells resulting in smaller TADs and altered gene expression profiles. The new TAD boundaries are commonly associated with copy-number changes observed in the cancer genome. We also identified new cancer-specific chromatin loops within TADs that are enriched for enhancers and pr...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b3228c85a81a7d93f1ebe62a7050ebdb" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953064,"asset_id":52927054,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953064/download_file?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="52927054"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927054"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927054; 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$(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="52927053"><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/52927053/Neurofilament_labeled_pyramidal_neurons_and_astrocytes_are_deficient_in_DNA_methylation_marks_in_Alzheimers_disease"><img alt="Research paper thumbnail of Neurofilament-labeled pyramidal neurons and astrocytes are deficient in DNA methylation marks in Alzheimer's disease" 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/52927053/Neurofilament_labeled_pyramidal_neurons_and_astrocytes_are_deficient_in_DNA_methylation_marks_in_Alzheimers_disease">Neurofilament-labeled pyramidal neurons and astrocytes are deficient in DNA methylation marks in Alzheimer's disease</a></div><div class="wp-workCard_item"><span>Neurobiology of Aging</span><span>, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">There is increasing evidence that epigenetic alterations may play a role in Alzheimer&amp;#39;s d...</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">There is increasing evidence that epigenetic alterations may play a role in Alzheimer&amp;#39;s disease (AD); yet, there is little information regarding epigenetic modifications in specific cell types. We assessed DNA methylation (5-methylcytosine [5mC]) and hydroxymethylation (5-hydroxymethylcytosine [5hmC]) marks specifically in neuronal and glial cell types in the inferior temporal gyrus of human AD cases and age-matched controls. Interestingly, neurofilament (NF)-labeled pyramidal neurons that are vulnerable to AD pathology are deficient in extranuclear 5mC in AD cases compared with controls. We also found that fewer astrocytes exhibited nuclear 5mC and 5hmC marks in AD cases compared with controls. However, there were no alterations in 5mC and 5hmC in disease-resistant calretinin interneurons or microglia in AD, and there was no alteration in the density of 5mC- or 5hmC-labeled nuclei in near-plaque versus plaque-free regions in late-AD cases. 5mC and 5hmC were present in a high proportion of neurofibrillary tangles, suggesting no loss of DNA methylation marks in tangle bearing neurons. We provide evidence that epigenetic dysregulation may be occurring in astrocytes and NF-positive pyramidal neurons in AD.</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="52927053"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927053"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927053; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927053]").text(description); 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</script> <div class="js-work-strip profile--work_container" data-work-id="52927052"><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/52927052/Three_dimensional_disorganisation_of_the_cancer_genome_occurs_coincident_with_long_range_genetic_and_epigenetic_alterations"><img alt="Research paper thumbnail of Three-dimensional disorganisation of the cancer genome occurs coincident with long range genetic and epigenetic alterations" class="work-thumbnail" src="https://attachments.academia-assets.com/69953058/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/52927052/Three_dimensional_disorganisation_of_the_cancer_genome_occurs_coincident_with_long_range_genetic_and_epigenetic_alterations">Three-dimensional disorganisation of the cancer genome occurs coincident with long range genetic and epigenetic alterations</a></div><div class="wp-workCard_item"><span>Genome Research</span><span>, 2016</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bfb2178ded6959bb53e24a77c0594adb" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953058,"asset_id":52927052,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953058/download_file?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="52927052"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927052"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927052; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="52927051"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/52927051/Cancer_Epigenetics"><img alt="Research paper thumbnail of Cancer Epigenetics" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/52927051/Cancer_Epigenetics">Cancer Epigenetics</a></div><div class="wp-workCard_item"><span>Drug Discovery in Cancer Epigenetics</span><span>, 2016</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="52927051"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927051"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927051; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927051]").text(description); $(".js-view-count[data-work-id=52927051]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927051; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927051']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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" } } $('.js-work-strip[data-work-id=52927051]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":52927051,"title":"Cancer Epigenetics","internal_url":"https://www.academia.edu/52927051/Cancer_Epigenetics","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[]}, 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="52927050"><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/52927050/Interplay_between_Transcription_Factors_and_the_Epigenome_Insight_from_the_Role_of_RUNX1_in_Leukemia"><img alt="Research paper thumbnail of Interplay between Transcription Factors and the Epigenome: Insight from the Role of RUNX1 in Leukemia" class="work-thumbnail" src="https://attachments.academia-assets.com/69953055/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/52927050/Interplay_between_Transcription_Factors_and_the_Epigenome_Insight_from_the_Role_of_RUNX1_in_Leukemia">Interplay between Transcription Factors and the Epigenome: Insight from the Role of RUNX1 in Leukemia</a></div><div class="wp-workCard_item"><span>Frontiers in Immunology</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The genome has the ability to respond in a precise and coordinated manner to cellular signals. It...</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 genome has the ability to respond in a precise and coordinated manner to cellular signals. It achieves this through the concerted actions of transcription factors and the chromatin platform, which are targets of the signaling pathways. Our understanding of the molecular mechanisms through which transcription factors and the chromatin landscape each control gene activity has expanded dramatically over recent years, and attention has now turned to understanding the complex, multifaceted interplay between these regulatory layers in normal and disease states. It has become apparent that transcription factors as well as the components and modifiers of the epigenetic machinery are frequent targets of genomic alterations in cancer cells. Through the study of these factors, we can gain unique insight into the dynamic interplay between transcription factors and the epigenome, and how their dysregulation leads to aberrant gene expression programs in cancer. Here, we will highlight how these factors normally cooperate to establish and maintain the transcriptional and epigenetic landscape of cells, and how this is reprogramed in cancer, focusing on the RUNX1 transcription factor and oncogenic derivative RUNX1-ETO in leukemia as paradigms of transcriptional and epigenetic reprograming.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a78e171e6374c88d393befdc188cd1c8" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953055,"asset_id":52927050,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953055/download_file?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="52927050"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927050"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927050; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "a78e171e6374c88d393befdc188cd1c8" } } $('.js-work-strip[data-work-id=52927050]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":52927050,"title":"Interplay between Transcription Factors and the Epigenome: Insight from the Role of RUNX1 in Leukemia","internal_url":"https://www.academia.edu/52927050/Interplay_between_Transcription_Factors_and_the_Epigenome_Insight_from_the_Role_of_RUNX1_in_Leukemia","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[{"id":69953055,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/69953055/thumbnails/1.jpg","file_name":"129bfac65778db666a7087d459829f2c3c3e.pdf","download_url":"https://www.academia.edu/attachments/69953055/download_file","bulk_download_file_name":"Interplay_between_Transcription_Factors.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/69953055/129bfac65778db666a7087d459829f2c3c3e-libre.pdf?1632116626=\u0026response-content-disposition=attachment%3B+filename%3DInterplay_between_Transcription_Factors.pdf\u0026Expires=1740014889\u0026Signature=bsHpd2cCP-puB3OFQ5raSTaKOd72e91mMlmlqIIt391Fav9inc5oLXR7iO3Zj0Hh7ZsOzq6GnYElRB706IPmG5vDzivpZ---GLI1IjgYs0HqQlL~QthEGQGXqP19asgjl9irJxXem-BYsNxF3iVivc~hDXDm2ZDftiUun7DGzmFuFDCwuXCecSv-OFN7Pmd5lNEHIjA9QUhSuTiaj0u41F4BCkCfym3lDf9bs7F-GV-1-U8FDoYRW1Z-e7-gXtO8yLwltgMYLYJMIMH~Zwny1Igsgz9kmVYRYaR2BLYxH481Zv0XMC6rrNAnAu4hWbdf5twFLpu7SVwLAG3qZqEqag__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, 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="52927049"><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/52927049/The_Leukemia_Inhibitory_Factor_Receptor_gene_is_a_direct_target_of_RUNX1"><img alt="Research paper thumbnail of The Leukemia Inhibitory Factor Receptor gene is a direct target of RUNX1" 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/52927049/The_Leukemia_Inhibitory_Factor_Receptor_gene_is_a_direct_target_of_RUNX1">The Leukemia Inhibitory Factor Receptor gene is a direct target of RUNX1</a></div><div class="wp-workCard_item"><span>Journal of Cellular Biochemistry</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Activation of cytokine signalling via the Leukemia Inhibitory Factor Receptor (LIFR) plays an int...</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">Activation of cytokine signalling via the Leukemia Inhibitory Factor Receptor (LIFR) plays an integral role in hematopoiesis, osteogenesis and placental development, along with mediating neurotrophic mechanisms. However the regulatory control of the LIFR gene has remained largely unexplored. Here we characterise the LIFR gene as a novel target of the RUNX1 transcription factor. The RUNX1 transcription factor is an essential regulator of hematopoiesis and is a frequent target of point mutations and chromosomal alterations in leukemia. RUNX1 regulates hematopoiesis through its control of genes important for hematopoietic cell growth, proliferation and differentiation, including a number of cytokines and cytokine receptors. LIFR is regulated by two alternate promoters, a placental-specific and a ubiquitously active general promoter. We show that both of these promoters are regulated by RUNX1. However, in myeloid cells LIFR expression is driven solely by the general LIFR promoter with our data indicating that the placental promoter is epigenetically silenced in these cells. While RUNX1 activates the LIFR general pr omoter, the oncogenic RUNX1-ETO fusion protein generated by the t(8;21) translocation commonly associated with acute myeloid leukemia represses promoter activity. The data presented here establish LIFR as a transcriptional target of RUNX1 and suggests that disruption of RUNX1 activity in myeloid cells may result in altered LIFR signalling in these cells. This article is protected by copyright. All rights reserved.</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="52927049"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927049"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927049; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927049]").text(description); $(".js-view-count[data-work-id=52927049]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927049; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927049']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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" } } $('.js-work-strip[data-work-id=52927049]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":52927049,"title":"The Leukemia Inhibitory Factor Receptor gene is a direct target of RUNX1","internal_url":"https://www.academia.edu/52927049/The_Leukemia_Inhibitory_Factor_Receptor_gene_is_a_direct_target_of_RUNX1","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[]}, 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="52927048"><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/52927048/Genome_wide_nucleosome_occupancy_and_DNA_methylation_profiling_of_four_human_cell_lines"><img alt="Research paper thumbnail of Genome-wide nucleosome occupancy and DNA methylation profiling of four human cell lines" class="work-thumbnail" src="https://attachments.academia-assets.com/69953059/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/52927048/Genome_wide_nucleosome_occupancy_and_DNA_methylation_profiling_of_four_human_cell_lines">Genome-wide nucleosome occupancy and DNA methylation profiling of four human cell lines</a></div><div class="wp-workCard_item"><span>Genomics Data</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">DNA methylation and nucleosome positioning are two key mechanisms that contribute to the epigenet...</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">DNA methylation and nucleosome positioning are two key mechanisms that contribute to the epigenetic control of gene expression. During carcinogenesis, the expression of many genes is altered alongside extensive changes in the epigenome, with repressed genes often being associated with local DNA hypermethylation and gain of nucleosomes at their promoters. However the spectrum of alterations that occur at distal regulatory regions has not been extensively studied. To address this we used Nucleosome Occupancy and Methylation sequencing (NOMe-seq) to compare the genome-wide DNA methylation and nucleosome occupancy profiles between normal and cancer cell line models of the breast and prostate. Here we describe the bioinformatic pipeline and methods that we developed for the processing and analysis of the NOMe-seq data published by (Taberlay et al., 2014 [1]) and deposited in the Gene Expression Omnibus with accession GSE57498.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="ac08a572539584d574057d3137e7957b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953059,"asset_id":52927048,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953059/download_file?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="52927048"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927048"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927048; 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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="52927047"><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/52927047/Chromatin_remodeler_mutations_in_human_cancers_epigenetic_implications"><img alt="Research paper thumbnail of Chromatin remodeler mutations in human cancers: epigenetic implications" class="work-thumbnail" src="https://attachments.academia-assets.com/69953075/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/52927047/Chromatin_remodeler_mutations_in_human_cancers_epigenetic_implications">Chromatin remodeler mutations in human cancers: epigenetic implications</a></div><div class="wp-workCard_item"><span>Epigenomics</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Chromatin remodeler complexes exhibit the ability to alter nucleosome composition and positions, ...</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">Chromatin remodeler complexes exhibit the ability to alter nucleosome composition and positions, with seemingly divergent roles in the regulation of chromatin architecture and gene expression. The outcome is directed by subunit variation and interactions with accessory factors. Recent studies have revealed that subunits of chromatin remodelers display an unexpectedly high mutation rate and/or are inactivated in a number of cancers. Consequently, a repertoire of epigenetic processes are likely to be affected, including interactions with histone modifying factors, as well as the ability to precisely modulate nucleosome positions, DNA methylation patterns and potentially, higher-order genome structure. However, the true significance of chromatin remodeler genetic aberrations in promoting a cascade of epigenetic changes, particularly during initiation and progression of cancer, remains largely unknown.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="8299533907ccfdc47d533ce06af845d4" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953075,"asset_id":52927047,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953075/download_file?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="52927047"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927047"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927047; 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$(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="11869565" id="papers"><div class="js-work-strip profile--work_container" data-work-id="69295950"><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/69295950/H3K4me3_enrichment_defines_neuronal_age_while_a_youthful_H3K27ac_signature_is_recapitulated_in_aged_neurons"><img alt="Research paper thumbnail of H3K4me3 enrichment defines neuronal age, while a youthful H3K27ac signature is recapitulated in aged neurons" 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/69295950/H3K4me3_enrichment_defines_neuronal_age_while_a_youthful_H3K27ac_signature_is_recapitulated_in_aged_neurons">H3K4me3 enrichment defines neuronal age, while a youthful H3K27ac signature is recapitulated in aged neurons</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ABSTRACTNeurons live for the lifespan of the individual and underlie our ability for lifelong lea...</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">ABSTRACTNeurons live for the lifespan of the individual and underlie our ability for lifelong learning and memory. However, aging alters neuron morphology and function resulting in age-related cognitive decline. It is well established that epigenetic alterations are essential for learning and memory, yet few neuron-specific genome-wide epigenetic maps exist into old age. Comprehensive mapping of H3K4me3 and H3K27ac in mouse neurons across lifespan revealed plastic H3K4me3 marking that differentiates neuronal age linked to known characteristics of cellular and neuronal aging. We determined that neurons in old age recapitulate the H3K27ac enrichment at promoters, enhancers and super enhancers from young adult neurons, likely representing a re-activation of pathways to maintain neuronal output. Finally, this study identified new characteristics of neuronal aging, including altered rDNA regulation and epigenetic regulatory mechanisms. Collectively, these findings indicate a key role for...</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="69295950"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="69295950"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 69295950; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=69295950]").text(description); $(".js-view-count[data-work-id=69295950]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 69295950; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='69295950']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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" } } $('.js-work-strip[data-work-id=69295950]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":69295950,"title":"H3K4me3 enrichment defines neuronal age, while a youthful H3K27ac signature is recapitulated in aged neurons","internal_url":"https://www.academia.edu/69295950/H3K4me3_enrichment_defines_neuronal_age_while_a_youthful_H3K27ac_signature_is_recapitulated_in_aged_neurons","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[]}, 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="58914884"><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/58914884/DNA_Methylation_and_Cancer"><img alt="Research paper thumbnail of DNA Methylation and Cancer" class="work-thumbnail" src="https://attachments.academia-assets.com/73094115/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/58914884/DNA_Methylation_and_Cancer">DNA Methylation and Cancer</a></div><div class="wp-workCard_item"><span>Journal of Clinical Oncology</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">DNA methylation acts in concert with other epigenetic mechanisms to regulate normal gene expressi...</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">DNA methylation acts in concert with other epigenetic mechanisms to regulate normal gene expression and facilitate chromatin organization within cells. Aberrant DNA methylation patterns are acquired during carcinogenic transformation; such events are often accompanied by alterations in chromatin structure at gene regulatory regions. The expression pattern of any given gene is achieved by interacting epigenetic mechanisms. First, the insertion of nucleosomes at transcriptional start sites prevents the binding of the transcriptional machinery and additional cofactors that initiate gene expression. Second, nucleosomes anchor all of the DNMT3A and DNMT3B methyltransferase proteins in the cell, which suggests a role for histone octamers in the establishment of DNA methylation patterns. During carcinogenesis, epigenetic switching and 5-methylcytosine reprogramming result in the aberrant hypermethylation of CpG islands, reducing epigenetic plasticity of critical developmental and tumor suppressor genes, rendering them unresponsive to normal stimuli. Here, we will discuss the importance of both established and novel molecular concepts that may underlie the role of DNA methylation in cancer.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b11a34ed857e2e629c92cab8014534da" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":73094115,"asset_id":58914884,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/73094115/download_file?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="58914884"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="58914884"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 58914884; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=58914884]").text(description); $(".js-view-count[data-work-id=58914884]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 58914884; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='58914884']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="52927064"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/52927064/Targeting_histone_acetylation_dynamics_and_oncogenic_transcription_by_catalytic_P300_CBP_inhibition"><img alt="Research paper thumbnail of Targeting histone acetylation dynamics and oncogenic transcription by catalytic P300/CBP inhibition" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/52927064/Targeting_histone_acetylation_dynamics_and_oncogenic_transcription_by_catalytic_P300_CBP_inhibition">Targeting histone acetylation dynamics and oncogenic transcription by catalytic P300/CBP inhibition</a></div><div class="wp-workCard_item"><span>Molecular Cell</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="52927064"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927064"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927064; 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</script> <div class="js-work-strip profile--work_container" data-work-id="52927063"><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/52927063/BRG1_knockdown_inhibits_proliferation_through_multiple_cellular_pathways_in_prostate_cancer"><img alt="Research paper thumbnail of BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer" class="work-thumbnail" src="https://attachments.academia-assets.com/69953008/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/52927063/BRG1_knockdown_inhibits_proliferation_through_multiple_cellular_pathways_in_prostate_cancer">BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer</a></div><div class="wp-workCard_item"><span>Clinical Epigenetics</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background BRG1 (encoded by SMARCA4) is a catalytic component of the SWI/SNF chromatin remodellin...</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">Background BRG1 (encoded by SMARCA4) is a catalytic component of the SWI/SNF chromatin remodelling complex, with key roles in modulating DNA accessibility. Dysregulation of BRG1 is observed, but functionally uncharacterised, in a wide range of malignancies. We have probed the functions of BRG1 on a background of prostate cancer to investigate how BRG1 controls gene expression programmes and cancer cell behaviour. Results Our investigation of SMARCA4 revealed that BRG1 is over-expressed in the majority of the 486 tumours from The Cancer Genome Atlas prostate cohort, as well as in a complementary panel of 21 prostate cell lines. Next, we utilised a temporal model of BRG1 depletion to investigate the molecular effects on global transcription programmes. Depleting BRG1 had no impact on alternative splicing and conferred only modest effect on global expression. However, of the transcriptional changes that occurred, most manifested as down-regulated expression. Deeper examination found th...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bec56653b7d3ffaf2b0cc5c3a465ab7f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953008,"asset_id":52927063,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953008/download_file?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="52927063"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927063"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927063; 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$(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="52927062"><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/52927062/BRG1_promotes_transcriptional_patterns_that_are_permissive_to_proliferation_in_cancer_cells"><img alt="Research paper thumbnail of BRG1 promotes transcriptional patterns that are permissive to proliferation in cancer cells" 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/52927062/BRG1_promotes_transcriptional_patterns_that_are_permissive_to_proliferation_in_cancer_cells">BRG1 promotes transcriptional patterns that are permissive to proliferation in cancer cells</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ABSTRACTBackgroundBRG1 (encoded bySMARCA4) is a catalytic component of the SWI/SNF chromatin remo...</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">ABSTRACTBackgroundBRG1 (encoded bySMARCA4) is a catalytic component of the SWI/SNF chromatin remodelling complex, with key roles in modulating DNA accessibility. Dysregulation of BRG1 is observed, but functionally uncharacterised, in a wide range of malignancies. We have probed the functions of BRG1 on a background of prostate cancer to investigate how BRG1 controls gene expression programs and cancer cell behaviour.ResultsOur investigation ofSMARCA4revealed that BRG1 is universally overexpressed in 486 tumours from The Cancer Genome Atlas prostate cohort, as well as in a complementary panel of 21 prostate cell lines. Next, we utilised a temporal model of BRG1 depletion to investigate the molecular effects on global transcription programs. Unexpectedly, depleting BRG1 had no impact on alternative splicing and conferred only modest effect on global expression. However, of the transcriptional changes that occurred, most manifested as down-regulated expression. Deeper examination found...</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="52927062"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927062"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927062; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927062]").text(description); $(".js-view-count[data-work-id=52927062]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927062; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927062']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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" } } $('.js-work-strip[data-work-id=52927062]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":52927062,"title":"BRG1 promotes transcriptional patterns that are permissive to proliferation in cancer cells","internal_url":"https://www.academia.edu/52927062/BRG1_promotes_transcriptional_patterns_that_are_permissive_to_proliferation_in_cancer_cells","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[]}, 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="52927061"><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/52927061/The_DNA_methylation_landscape_in_cancer"><img alt="Research paper thumbnail of The DNA methylation landscape in cancer" class="work-thumbnail" src="https://attachments.academia-assets.com/69953012/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/52927061/The_DNA_methylation_landscape_in_cancer">The DNA methylation landscape in cancer</a></div><div class="wp-workCard_item"><span>Essays in Biochemistry</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">As one of the most abundant and well-studied epigenetic modifications, DNA methylation plays an e...</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">As one of the most abundant and well-studied epigenetic modifications, DNA methylation plays an essential role in normal development and cellular biology. Global alterations to the DNA methylation landscape contribute to alterations in the transcriptome and deregulation of cellular pathways. Indeed, improved methods to study DNA methylation patterning and dynamics at base pair resolution and across individual DNA molecules on a genome-wide scale has highlighted the scope of change to the DNA methylation landscape in disease states, particularly during tumorigenesis. More recently has been the development of DNA hydroxymethylation profiling techniques, which allows differentiation between 5mC and 5hmC profiles and provides further insights into DNA methylation dynamics and remodeling in tumorigenesis. In this review, we describe the distribution of DNA methylation and DNA hydroxymethylation in different genomic contexts, first in normal cells, and how this is altered in cancer. Final...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="863591c750fe19b11c881f6de8a8c2d3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953012,"asset_id":52927061,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953012/download_file?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="52927061"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927061"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927061; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927061]").text(description); $(".js-view-count[data-work-id=52927061]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927061; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927061']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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: "863591c750fe19b11c881f6de8a8c2d3" } } $('.js-work-strip[data-work-id=52927061]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":52927061,"title":"The DNA methylation landscape in cancer","internal_url":"https://www.academia.edu/52927061/The_DNA_methylation_landscape_in_cancer","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[{"id":69953012,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/69953012/thumbnails/1.jpg","file_name":"ebc-2019-0037c.pdf","download_url":"https://www.academia.edu/attachments/69953012/download_file","bulk_download_file_name":"The_DNA_methylation_landscape_in_cancer.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/69953012/ebc-2019-0037c-libre.pdf?1632116630=\u0026response-content-disposition=attachment%3B+filename%3DThe_DNA_methylation_landscape_in_cancer.pdf\u0026Expires=1740014889\u0026Signature=Mht1bcoBPZHdcinjqSPgp3~iiRunjwxxDnGMLr3r2v2PanLsD8wGmTBVJO~9w5hZnmEEEf308N5h84CFZPX4QaHgjnMVa3FNW~Q019Q9eduvJru-0h85hFmYZ9R8lepoNkQhMkwuLWxq4Y4Jh9MGqzi9y2jE-dxP0dnwhZOXMGoAQc~~QRvlJyu-SDNuA2d0cH26gI7Jgv4k1crlqME-QEz6rNPEf6ZPXYsoH8jZwwEKDCo6HvAcxCVA2tB4IAqV-2PY8k6Z-LkjXid0lvEJn23dMAEY0rcHWGNdBUSRqF5YhlIy1nmaPKEVN--s9chGuKs0JVUnlOY~C0j1omnIUA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, 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="52927060"><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/52927060/Constitutively_bound_CTCF_sites_maintain_3D_chromatin_architecture_and_long_range_epigenetically_regulated_domains"><img alt="Research paper thumbnail of Constitutively bound CTCF sites maintain 3D chromatin architecture and long-range epigenetically regulated domains" class="work-thumbnail" src="https://attachments.academia-assets.com/69953015/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/52927060/Constitutively_bound_CTCF_sites_maintain_3D_chromatin_architecture_and_long_range_epigenetically_regulated_domains">Constitutively bound CTCF sites maintain 3D chromatin architecture and long-range epigenetically regulated domains</a></div><div class="wp-workCard_item"><span>Nature Communications</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The architectural protein CTCF is a mediator of chromatin conformation, but how CTCF binding to D...</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 architectural protein CTCF is a mediator of chromatin conformation, but how CTCF binding to DNA is orchestrated to maintain long-range gene expression is poorly understood. Here we perform RNAi knockdown to reduce CTCF levels and reveal a shared subset of CTCF-bound sites are robustly resistant to protein depletion. The ‘persistent’ CTCF sites are enriched at domain boundaries and chromatin loops constitutive to all cell types. CRISPR-Cas9 deletion of 2 persistent CTCF sites at the boundary between a long-range epigenetically active (LREA) and silenced (LRES) region, within the Kallikrein (KLK) locus, results in concordant activation of all 8 KLK genes within the LRES region. CTCF genome-wide depletion results in alteration in Topologically Associating Domain (TAD) structure, including the merging of TADs, whereas TAD boundaries are not altered where persistent sites are maintained. We propose that the subset of essential CTCF sites are involved in cell-type constitutive, higher...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="87c42288c15366176f58facfbd1c3f8b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953015,"asset_id":52927060,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953015/download_file?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="52927060"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927060"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927060; 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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="52927059"><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/52927059/Xmas_ESC_A_new_female_embryonic_stem_cell_system_that_reveals_the_BAF_complex_as_a_key_regulator_of_the_establishment_of_X_chromosome_inactivation"><img alt="Research paper thumbnail of Xmas ESC: A new female embryonic stem cell system that reveals the BAF complex as a key regulator of the establishment of X chromosome inactivation" class="work-thumbnail" src="https://attachments.academia-assets.com/69953056/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/52927059/Xmas_ESC_A_new_female_embryonic_stem_cell_system_that_reveals_the_BAF_complex_as_a_key_regulator_of_the_establishment_of_X_chromosome_inactivation">Xmas ESC: A new female embryonic stem cell system that reveals the BAF complex as a key regulator of the establishment of X chromosome inactivation</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Although female pluripotency significantly differs to male, complications with in vitro culture o...</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">Although female pluripotency significantly differs to male, complications with in vitro culture of female embryonic stem cells (ESC) have severely limited the use and study of these cells. We report a replenishable female ESC system, Xmas, that has enabled us to optimise a protocol for preserving the XX karyotype. Our protocol also improves male ESC fitness. We utilised our Xmas ESC system to screen for regulators of the female-specific process of X chromosome inactivation, revealing chromatin remodellers Smarcc1 and Smarca4 as key regulators of establishment of X inactivation. The remodellers create a nucleosome depleted region at gene promotors on the inactive X during exit from pluripotency, without which gene silencing fails. Our female ESC system provides a tractable model for XX ESC culture that will expedite study of female pluripotency and has enabled us to discover new features of the female-specific process of X inactivation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="e68ecdf959371ce9638ce92dd8a61268" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953056,"asset_id":52927059,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953056/download_file?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="52927059"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927059"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927059; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927059]").text(description); $(".js-view-count[data-work-id=52927059]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927059; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927059']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(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="52927058"><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/52927058/DNA_methylation_changes_following_DNA_damage_in_prostate_cancer_cells"><img alt="Research paper thumbnail of DNA methylation changes following DNA damage in prostate cancer cells" class="work-thumbnail" src="https://attachments.academia-assets.com/69953007/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/52927058/DNA_methylation_changes_following_DNA_damage_in_prostate_cancer_cells">DNA methylation changes following DNA damage in prostate cancer cells</a></div><div class="wp-workCard_item"><span>Epigenetics</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Many cancer therapies operate by inducing double-strand breaks (DSBs) in cancer cells, however tr...</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">Many cancer therapies operate by inducing double-strand breaks (DSBs) in cancer cells, however treatment-resistant cells rapidly initiate mechanisms to repair damage enabling survival. While the DNA repair mechanisms responsible for cancer cell survival following DNA damaging treatments are becoming better understood, less is known about the role of the epigenome in this process. Using prostate cancer cell lines with differing sensitivities to radiation treatment, we analysed the DNA methylation profiles prior to and following a single dose of radiotherapy (RT) using the Illumina Infinium HumanMethylation450 BeadChip platform. DSB formation and repair, in the absence and presence of the DNA hypomethylating agent, 5-azacytidine (5-AzaC), were also investigated using γH2A.X immunofluorescence staining. Here we demonstrate that DNA methylation is generally stable following a single dose of RT; however, a small number of CpG sites are stably altered up to 14 d following exposure. While the radioresistant and radiosensitive cells displayed distinct basal DNA methylation profiles, their susceptibility to DNA damage appeared similar demonstrating that basal DNA methylation has a limited influence on DSB induction at the regions examined. Recovery from DSB induction was also similar between these cells. Treatment with 5-AzaC did not sensitize resistant cells to DNA damage, but rather delayed recruitment of phosphorylated BRCA1 (S1423) and repair of DSBs. These results highlight that stable epigenetic changes are possible following a single dose of RT and may have significant clinical implications for cancer treatment involving recurrent or fractionated dosing regimens.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="8ea5c009eeb592153983d230e417d719" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953007,"asset_id":52927058,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953007/download_file?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="52927058"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927058"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927058; 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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="52927057"><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/52927057/Age_but_Not_Amyloidosis_Induced_Changes_in_Global_Levels_of_Histone_Modifications_in_Susceptible_and_Disease_Resistant_Neurons_in_Alzheimer_s_Disease_Model_Mice"><img alt="Research paper thumbnail of Age, but Not Amyloidosis, Induced Changes in Global Levels of Histone Modifications in Susceptible and Disease-Resistant Neurons in Alzheimer’s Disease Model Mice" class="work-thumbnail" src="https://attachments.academia-assets.com/69953057/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/52927057/Age_but_Not_Amyloidosis_Induced_Changes_in_Global_Levels_of_Histone_Modifications_in_Susceptible_and_Disease_Resistant_Neurons_in_Alzheimer_s_Disease_Model_Mice">Age, but Not Amyloidosis, Induced Changes in Global Levels of Histone Modifications in Susceptible and Disease-Resistant Neurons in Alzheimer’s Disease Model Mice</a></div><div class="wp-workCard_item"><span>Frontiers in Aging Neuroscience</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">There is increasing interest in the role of epigenetic alterations in Alzheimer's disease (AD). T...</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">There is increasing interest in the role of epigenetic alterations in Alzheimer's disease (AD). The epigenome of every cell type is distinct, yet data regarding epigenetic change in specific cell types in aging and AD is limited. We investigated histone tail modifications in neuronal subtypes in wild-type and APP/PS1 mice at 3 (prepathology), 6 (pathology-onset) and 12 (pathology-rich) months of age. In neurofilament (NF)-positive pyramidal neurons (vulnerable to AD pathology), and in calretinin-labeled interneurons (resistant to AD pathology) there were no global alterations in histone 3 lysine 4 trimethylation (H3K4me3), histone 3 lysine 27 acetylation (H3K27ac) or histone 3 lysine 27 trimethylation (H3K27me3) in APP/PS1 compared to wild-type mice at any age. Interestingly, age-related changes in the presence of H3K27ac and H3K27me3 were detected in NF-labeled pyramidal neurons and calretinin-positive interneurons, respectively. These data suggest that the global levels of histone modifications change with age, whilst amyloid plaque deposition and its sequelae do not result in global alterations of H3K4me3, H3K27ac and H3K27me3 in NF-positive pyramidal neurons or calretinin-labeled interneurons.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="856b6d583adda0816f024e25bb4d1f15" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953057,"asset_id":52927057,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953057/download_file?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="52927057"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927057"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927057; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927057]").text(description); $(".js-view-count[data-work-id=52927057]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927057; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927057']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(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="52927056"><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/52927056/Integrated_epigenomic_analysis_stratifies_chromatin_remodellers_into_distinct_functional_groups"><img alt="Research paper thumbnail of Integrated epigenomic analysis stratifies chromatin remodellers into distinct functional groups" class="work-thumbnail" src="https://attachments.academia-assets.com/69953004/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/52927056/Integrated_epigenomic_analysis_stratifies_chromatin_remodellers_into_distinct_functional_groups">Integrated epigenomic analysis stratifies chromatin remodellers into distinct functional groups</a></div><div class="wp-workCard_item"><span>Epigenetics & Chromatin</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background: ATP-dependent chromatin remodelling complexes are responsible for establishing and ma...</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">Background: ATP-dependent chromatin remodelling complexes are responsible for establishing and maintaining the positions of nucleosomes. Chromatin remodellers are targeted to chromatin by transcription factors and noncoding RNA to remodel the chromatin into functional states. However, the influence of chromatin remodelling on shaping the functional epigenome is not well understood. Moreover, chromatin remodellers have not been extensively explored as a collective group across two-dimensional and three-dimensional epigenomic layers. Results: Here, we have integrated the genome-wide binding profiles of eight chromatin remodellers together with DNA methylation, nucleosome positioning, histone modification and Hi-C chromosomal contacts to reveal that chromatin remodellers can be stratified into two functional groups. Group 1 (BRG1, SNF2H, CHD3 and CHD4) has a clear preference for binding at 'actively marked' chromatin and Group 2 (BRM, INO80, SNF2L and CHD1) for 'repressively marked' chromatin. We find that histone modifications and chromatin architectural features, but not DNA methylation, stratify the remodellers into these functional groups. Conclusions: Our findings suggest that chromatin remodelling events are synchronous and that chromatin remodellers themselves should be considered simultaneously and not as individual entities in isolation or necessarily by structural similarity, as they are traditionally classified. Their coordinated function should be considered by preference for chromatin features in order to gain a more accurate and comprehensive picture of chromatin regulation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="41c2306ff8249ba5c5d37c1d2369cc52" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953004,"asset_id":52927056,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953004/download_file?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="52927056"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927056"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927056; 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Please cite this article as</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="e4f0a355d319360e2b65f76815b66e3b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953060,"asset_id":52927055,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953060/download_file?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="52927055"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927055"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927055; 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$(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="52927054"><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/52927054/Alterations_in_Three_Dimensional_Organization_of_the_Cancer_Genome_and_Epigenome"><img alt="Research paper thumbnail of Alterations in Three-Dimensional Organization of the Cancer Genome and Epigenome" class="work-thumbnail" src="https://attachments.academia-assets.com/69953064/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/52927054/Alterations_in_Three_Dimensional_Organization_of_the_Cancer_Genome_and_Epigenome">Alterations in Three-Dimensional Organization of the Cancer Genome and Epigenome</a></div><div class="wp-workCard_item"><span>Cold Spring Harbor symposia on quantitative biology</span><span>, Jan 19, 2017</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The structural and functional basis of the genome is provided by the three-dimensional (3D) chrom...</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 structural and functional basis of the genome is provided by the three-dimensional (3D) chromatin state. To enable accurate gene regulation, enhancer elements and promoter regions are brought into close spatial proximity to ensure proper, cell type-specific gene expression. In cancer, genetic and epigenetic processes can deregulate the transcriptional program. To investigate whether the 3D chromatin state is also disrupted in cancer we performed Hi-C chromosome conformation sequencing in normal and prostate cancer cells and compared the chromatin interaction maps with changes to the genome and epigenome. Notably, we find that additional topologically associated domain (TAD) boundaries are formed in cancer cells resulting in smaller TADs and altered gene expression profiles. The new TAD boundaries are commonly associated with copy-number changes observed in the cancer genome. We also identified new cancer-specific chromatin loops within TADs that are enriched for enhancers and pr...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b3228c85a81a7d93f1ebe62a7050ebdb" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953064,"asset_id":52927054,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953064/download_file?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="52927054"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927054"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927054; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927054]").text(description); $(".js-view-count[data-work-id=52927054]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927054; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927054']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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: "b3228c85a81a7d93f1ebe62a7050ebdb" } } $('.js-work-strip[data-work-id=52927054]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":52927054,"title":"Alterations in Three-Dimensional Organization of the Cancer Genome and Epigenome","internal_url":"https://www.academia.edu/52927054/Alterations_in_Three_Dimensional_Organization_of_the_Cancer_Genome_and_Epigenome","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[{"id":69953064,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/69953064/thumbnails/1.jpg","file_name":"118646_Journal_Article.pdf","download_url":"https://www.academia.edu/attachments/69953064/download_file","bulk_download_file_name":"Alterations_in_Three_Dimensional_Organiz.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/69953064/118646_Journal_Article-libre.pdf?1632116625=\u0026response-content-disposition=attachment%3B+filename%3DAlterations_in_Three_Dimensional_Organiz.pdf\u0026Expires=1740014889\u0026Signature=bAyDyfTbeat0AT-Izy40p2mxe9CZUJ~anNljO6NU8IWzDLHViR9HikodpRU4noMgJ8FIDiSCX8EPgbDGg9CeUNyWGmtey45jCr4QfNI5x~RriFrSIWzz8Z2hb7VTpl0ZVR1O2se6H1E3H5dmbVFcnXRFdM6c~iTfHOgvM8kS7IfJejnQ2AmP0Ens20XUBeud8znsIlFigBTG-7l2PyDShWkeeELcWqNucqaxMvO2mNhXdTFVktSBEHJWgj6GNrjVjgmL9S38puPfnY4qmWLYHfmlYxHxY7fohSaiwvD93aca1BVwSzNtTU-b3gWH1NZ88iwtSpZ9O8OPCmrRKz-QRQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, 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="52927053"><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/52927053/Neurofilament_labeled_pyramidal_neurons_and_astrocytes_are_deficient_in_DNA_methylation_marks_in_Alzheimers_disease"><img alt="Research paper thumbnail of Neurofilament-labeled pyramidal neurons and astrocytes are deficient in DNA methylation marks in Alzheimer's disease" 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/52927053/Neurofilament_labeled_pyramidal_neurons_and_astrocytes_are_deficient_in_DNA_methylation_marks_in_Alzheimers_disease">Neurofilament-labeled pyramidal neurons and astrocytes are deficient in DNA methylation marks in Alzheimer's disease</a></div><div class="wp-workCard_item"><span>Neurobiology of Aging</span><span>, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">There is increasing evidence that epigenetic alterations may play a role in Alzheimer&amp;#39;s d...</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">There is increasing evidence that epigenetic alterations may play a role in Alzheimer&amp;#39;s disease (AD); yet, there is little information regarding epigenetic modifications in specific cell types. We assessed DNA methylation (5-methylcytosine [5mC]) and hydroxymethylation (5-hydroxymethylcytosine [5hmC]) marks specifically in neuronal and glial cell types in the inferior temporal gyrus of human AD cases and age-matched controls. Interestingly, neurofilament (NF)-labeled pyramidal neurons that are vulnerable to AD pathology are deficient in extranuclear 5mC in AD cases compared with controls. We also found that fewer astrocytes exhibited nuclear 5mC and 5hmC marks in AD cases compared with controls. However, there were no alterations in 5mC and 5hmC in disease-resistant calretinin interneurons or microglia in AD, and there was no alteration in the density of 5mC- or 5hmC-labeled nuclei in near-plaque versus plaque-free regions in late-AD cases. 5mC and 5hmC were present in a high proportion of neurofibrillary tangles, suggesting no loss of DNA methylation marks in tangle bearing neurons. We provide evidence that epigenetic dysregulation may be occurring in astrocytes and NF-positive pyramidal neurons in AD.</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="52927053"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927053"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927053; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927053]").text(description); 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</script> <div class="js-work-strip profile--work_container" data-work-id="52927052"><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/52927052/Three_dimensional_disorganisation_of_the_cancer_genome_occurs_coincident_with_long_range_genetic_and_epigenetic_alterations"><img alt="Research paper thumbnail of Three-dimensional disorganisation of the cancer genome occurs coincident with long range genetic and epigenetic alterations" class="work-thumbnail" src="https://attachments.academia-assets.com/69953058/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/52927052/Three_dimensional_disorganisation_of_the_cancer_genome_occurs_coincident_with_long_range_genetic_and_epigenetic_alterations">Three-dimensional disorganisation of the cancer genome occurs coincident with long range genetic and epigenetic alterations</a></div><div class="wp-workCard_item"><span>Genome Research</span><span>, 2016</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bfb2178ded6959bb53e24a77c0594adb" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953058,"asset_id":52927052,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953058/download_file?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="52927052"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927052"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927052; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927052]").text(description); $(".js-view-count[data-work-id=52927052]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927052; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927052']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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: "bfb2178ded6959bb53e24a77c0594adb" } } $('.js-work-strip[data-work-id=52927052]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":52927052,"title":"Three-dimensional disorganisation of the cancer genome occurs coincident with long range genetic and epigenetic alterations","internal_url":"https://www.academia.edu/52927052/Three_dimensional_disorganisation_of_the_cancer_genome_occurs_coincident_with_long_range_genetic_and_epigenetic_alterations","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[{"id":69953058,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/69953058/thumbnails/1.jpg","file_name":"9eff60385732b1a7acf3373e2bcf4d75ce02.pdf","download_url":"https://www.academia.edu/attachments/69953058/download_file","bulk_download_file_name":"Three_dimensional_disorganisation_of_the.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/69953058/9eff60385732b1a7acf3373e2bcf4d75ce02-libre.pdf?1632116624=\u0026response-content-disposition=attachment%3B+filename%3DThree_dimensional_disorganisation_of_the.pdf\u0026Expires=1740014889\u0026Signature=b8OVU9x2vCbwHBJtURR1VPZM6oJXHfWr4ZFD5J4NSV-J~hGr-1AslSx82D-gstAd3Xq~-bINzqYyFKTOKoc-aTr6yrKoVeW4eAkRQ1AuPqVrvDZB-YPKOlqjsvaUxT-eid82jxoQqBTPmGs65PaoOwbSSK6ZxqHMoAhPrSiHI2IpzUja8rx7LFy6C7iYza66IXRuL-B3t16qOnvAMHrB7VN3WzZVqvBfAxe-YmjRam4uBW7DS1~YSeQE9shy2JgQ~eZGWraJJBnFQktrcub-OCUyTCDPHCOjl26mYo~9i6b4NI3dEF17pKatNKmfPEoYzmkdhSVDwA~7fUt2yd75AQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="52927051"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/52927051/Cancer_Epigenetics"><img alt="Research paper thumbnail of Cancer Epigenetics" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/52927051/Cancer_Epigenetics">Cancer Epigenetics</a></div><div class="wp-workCard_item"><span>Drug Discovery in Cancer Epigenetics</span><span>, 2016</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="52927051"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927051"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927051; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927051]").text(description); $(".js-view-count[data-work-id=52927051]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927051; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927051']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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" } } $('.js-work-strip[data-work-id=52927051]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":52927051,"title":"Cancer Epigenetics","internal_url":"https://www.academia.edu/52927051/Cancer_Epigenetics","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[]}, 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="52927050"><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/52927050/Interplay_between_Transcription_Factors_and_the_Epigenome_Insight_from_the_Role_of_RUNX1_in_Leukemia"><img alt="Research paper thumbnail of Interplay between Transcription Factors and the Epigenome: Insight from the Role of RUNX1 in Leukemia" class="work-thumbnail" src="https://attachments.academia-assets.com/69953055/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/52927050/Interplay_between_Transcription_Factors_and_the_Epigenome_Insight_from_the_Role_of_RUNX1_in_Leukemia">Interplay between Transcription Factors and the Epigenome: Insight from the Role of RUNX1 in Leukemia</a></div><div class="wp-workCard_item"><span>Frontiers in Immunology</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The genome has the ability to respond in a precise and coordinated manner to cellular signals. It...</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 genome has the ability to respond in a precise and coordinated manner to cellular signals. It achieves this through the concerted actions of transcription factors and the chromatin platform, which are targets of the signaling pathways. Our understanding of the molecular mechanisms through which transcription factors and the chromatin landscape each control gene activity has expanded dramatically over recent years, and attention has now turned to understanding the complex, multifaceted interplay between these regulatory layers in normal and disease states. It has become apparent that transcription factors as well as the components and modifiers of the epigenetic machinery are frequent targets of genomic alterations in cancer cells. Through the study of these factors, we can gain unique insight into the dynamic interplay between transcription factors and the epigenome, and how their dysregulation leads to aberrant gene expression programs in cancer. Here, we will highlight how these factors normally cooperate to establish and maintain the transcriptional and epigenetic landscape of cells, and how this is reprogramed in cancer, focusing on the RUNX1 transcription factor and oncogenic derivative RUNX1-ETO in leukemia as paradigms of transcriptional and epigenetic reprograming.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a78e171e6374c88d393befdc188cd1c8" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953055,"asset_id":52927050,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953055/download_file?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="52927050"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927050"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927050; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927050]").text(description); $(".js-view-count[data-work-id=52927050]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927050; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927050']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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: "a78e171e6374c88d393befdc188cd1c8" } } $('.js-work-strip[data-work-id=52927050]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":52927050,"title":"Interplay between Transcription Factors and the Epigenome: Insight from the Role of RUNX1 in Leukemia","internal_url":"https://www.academia.edu/52927050/Interplay_between_Transcription_Factors_and_the_Epigenome_Insight_from_the_Role_of_RUNX1_in_Leukemia","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[{"id":69953055,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/69953055/thumbnails/1.jpg","file_name":"129bfac65778db666a7087d459829f2c3c3e.pdf","download_url":"https://www.academia.edu/attachments/69953055/download_file","bulk_download_file_name":"Interplay_between_Transcription_Factors.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/69953055/129bfac65778db666a7087d459829f2c3c3e-libre.pdf?1632116626=\u0026response-content-disposition=attachment%3B+filename%3DInterplay_between_Transcription_Factors.pdf\u0026Expires=1740014889\u0026Signature=bsHpd2cCP-puB3OFQ5raSTaKOd72e91mMlmlqIIt391Fav9inc5oLXR7iO3Zj0Hh7ZsOzq6GnYElRB706IPmG5vDzivpZ---GLI1IjgYs0HqQlL~QthEGQGXqP19asgjl9irJxXem-BYsNxF3iVivc~hDXDm2ZDftiUun7DGzmFuFDCwuXCecSv-OFN7Pmd5lNEHIjA9QUhSuTiaj0u41F4BCkCfym3lDf9bs7F-GV-1-U8FDoYRW1Z-e7-gXtO8yLwltgMYLYJMIMH~Zwny1Igsgz9kmVYRYaR2BLYxH481Zv0XMC6rrNAnAu4hWbdf5twFLpu7SVwLAG3qZqEqag__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, 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="52927049"><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/52927049/The_Leukemia_Inhibitory_Factor_Receptor_gene_is_a_direct_target_of_RUNX1"><img alt="Research paper thumbnail of The Leukemia Inhibitory Factor Receptor gene is a direct target of RUNX1" 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/52927049/The_Leukemia_Inhibitory_Factor_Receptor_gene_is_a_direct_target_of_RUNX1">The Leukemia Inhibitory Factor Receptor gene is a direct target of RUNX1</a></div><div class="wp-workCard_item"><span>Journal of Cellular Biochemistry</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Activation of cytokine signalling via the Leukemia Inhibitory Factor Receptor (LIFR) plays an int...</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">Activation of cytokine signalling via the Leukemia Inhibitory Factor Receptor (LIFR) plays an integral role in hematopoiesis, osteogenesis and placental development, along with mediating neurotrophic mechanisms. However the regulatory control of the LIFR gene has remained largely unexplored. Here we characterise the LIFR gene as a novel target of the RUNX1 transcription factor. The RUNX1 transcription factor is an essential regulator of hematopoiesis and is a frequent target of point mutations and chromosomal alterations in leukemia. RUNX1 regulates hematopoiesis through its control of genes important for hematopoietic cell growth, proliferation and differentiation, including a number of cytokines and cytokine receptors. LIFR is regulated by two alternate promoters, a placental-specific and a ubiquitously active general promoter. We show that both of these promoters are regulated by RUNX1. However, in myeloid cells LIFR expression is driven solely by the general LIFR promoter with our data indicating that the placental promoter is epigenetically silenced in these cells. While RUNX1 activates the LIFR general pr omoter, the oncogenic RUNX1-ETO fusion protein generated by the t(8;21) translocation commonly associated with acute myeloid leukemia represses promoter activity. The data presented here establish LIFR as a transcriptional target of RUNX1 and suggests that disruption of RUNX1 activity in myeloid cells may result in altered LIFR signalling in these cells. This article is protected by copyright. All rights reserved.</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="52927049"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927049"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927049; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927049]").text(description); $(".js-view-count[data-work-id=52927049]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927049; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927049']"); 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></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.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" } } $('.js-work-strip[data-work-id=52927049]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":52927049,"title":"The Leukemia Inhibitory Factor Receptor gene is a direct target of RUNX1","internal_url":"https://www.academia.edu/52927049/The_Leukemia_Inhibitory_Factor_Receptor_gene_is_a_direct_target_of_RUNX1","owner_id":48659701,"coauthors_can_edit":true,"owner":{"id":48659701,"first_name":"Phillippa","middle_initials":null,"last_name":"Taberlay","page_name":"PhillippaTaberlay","domain_name":"independent","created_at":"2016-05-12T23:15:50.709-07:00","display_name":"Phillippa Taberlay","url":"https://independent.academia.edu/PhillippaTaberlay"},"attachments":[]}, 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="52927048"><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/52927048/Genome_wide_nucleosome_occupancy_and_DNA_methylation_profiling_of_four_human_cell_lines"><img alt="Research paper thumbnail of Genome-wide nucleosome occupancy and DNA methylation profiling of four human cell lines" class="work-thumbnail" src="https://attachments.academia-assets.com/69953059/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/52927048/Genome_wide_nucleosome_occupancy_and_DNA_methylation_profiling_of_four_human_cell_lines">Genome-wide nucleosome occupancy and DNA methylation profiling of four human cell lines</a></div><div class="wp-workCard_item"><span>Genomics Data</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">DNA methylation and nucleosome positioning are two key mechanisms that contribute to the epigenet...</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">DNA methylation and nucleosome positioning are two key mechanisms that contribute to the epigenetic control of gene expression. During carcinogenesis, the expression of many genes is altered alongside extensive changes in the epigenome, with repressed genes often being associated with local DNA hypermethylation and gain of nucleosomes at their promoters. However the spectrum of alterations that occur at distal regulatory regions has not been extensively studied. To address this we used Nucleosome Occupancy and Methylation sequencing (NOMe-seq) to compare the genome-wide DNA methylation and nucleosome occupancy profiles between normal and cancer cell line models of the breast and prostate. Here we describe the bioinformatic pipeline and methods that we developed for the processing and analysis of the NOMe-seq data published by (Taberlay et al., 2014 [1]) and deposited in the Gene Expression Omnibus with accession GSE57498.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="ac08a572539584d574057d3137e7957b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953059,"asset_id":52927048,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953059/download_file?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="52927048"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927048"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927048; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=52927048]").text(description); $(".js-view-count[data-work-id=52927048]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 52927048; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='52927048']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(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="52927047"><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/52927047/Chromatin_remodeler_mutations_in_human_cancers_epigenetic_implications"><img alt="Research paper thumbnail of Chromatin remodeler mutations in human cancers: epigenetic implications" class="work-thumbnail" src="https://attachments.academia-assets.com/69953075/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/52927047/Chromatin_remodeler_mutations_in_human_cancers_epigenetic_implications">Chromatin remodeler mutations in human cancers: epigenetic implications</a></div><div class="wp-workCard_item"><span>Epigenomics</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Chromatin remodeler complexes exhibit the ability to alter nucleosome composition and positions, ...</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">Chromatin remodeler complexes exhibit the ability to alter nucleosome composition and positions, with seemingly divergent roles in the regulation of chromatin architecture and gene expression. The outcome is directed by subunit variation and interactions with accessory factors. Recent studies have revealed that subunits of chromatin remodelers display an unexpectedly high mutation rate and/or are inactivated in a number of cancers. Consequently, a repertoire of epigenetic processes are likely to be affected, including interactions with histone modifying factors, as well as the ability to precisely modulate nucleosome positions, DNA methylation patterns and potentially, higher-order genome structure. However, the true significance of chromatin remodeler genetic aberrations in promoting a cascade of epigenetic changes, particularly during initiation and progression of cancer, remains largely unknown.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="8299533907ccfdc47d533ce06af845d4" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":69953075,"asset_id":52927047,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/69953075/download_file?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="52927047"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="52927047"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 52927047; 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