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href="https://irbbarcelona.academia.edu/IvanBarcoBarrantes">Ivan Barco Barrantes</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">IRB Barcelona</p></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a href="https://irbbarcelona.academia.edu/CarmeCortina"><img class="profile-avatar u-positionAbsolute" border="0" alt="" src="//a.academia-assets.com/images/s200_no_pic.png" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://irbbarcelona.academia.edu/CarmeCortina">Carme Cortina</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">IRB Barcelona</p></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a href="https://ub.academia.edu/SergioPalomo"><img class="profile-avatar u-positionAbsolute" border="0" alt="" 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href="https://uel.academia.edu/JanaJavornik">Jana Javornik</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">University of East London</p></div></div></ul></div><div class="ri-section"><div class="ri-section-header"><span>Interests</span></div><div class="ri-tags-container"><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="33247403" href="https://www.academia.edu/Documents/in/Centro_de_Investigaciones_Biologicas"><div id="js-react-on-rails-context" style="display:none" data-rails-context="{"inMailer":false,"i18nLocale":"en","i18nDefaultLocale":"en","href":"https://csic.academia.edu/CarmeloBernabeu","location":"/CarmeloBernabeu","scheme":"https","host":"csic.academia.edu","port":null,"pathname":"/CarmeloBernabeu","search":null,"httpAcceptLanguage":null,"serverSide":false}"></div> <div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Centro de 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data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/115437739/Abstract_6158_The_relevance_of_endoglin_and_MMP14_to_the_metastatic_potential_of_Ewing_sarcoma_cells"><img alt="Research paper thumbnail of Abstract 6158: The relevance of endoglin and MMP14 to the metastatic potential of Ewing sarcoma 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/115437739/Abstract_6158_The_relevance_of_endoglin_and_MMP14_to_the_metastatic_potential_of_Ewing_sarcoma_cells">Abstract 6158: The relevance of endoglin and MMP14 to the metastatic potential of Ewing sarcoma cells</a></div><div class="wp-workCard_item"><span>Tumor Biology</span><span>, Aug 13, 2020</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background: Ewing sarcoma (ES) is a developmental bone/soft tissue neoplasia, for which mesenchym...</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: Ewing sarcoma (ES) is a developmental bone/soft tissue neoplasia, for which mesenchymal stem cell (MSC) is the putative cell of origin. Although the outcome of ES patients bearing primary tumors has improved significantly, patients with metastatic ES still have a poor prognosis. The MSC marker endoglin/CD105 (ENG) and the ENG-shedding protease MMP14 have been, respectively, described as cell migration and invasion regulators. In our attempt to better understand the mechanism of ES progression, we are focusing on the role of ENG and MMP14 in ES cells. Methods: In vitro ENG-knockdown (ENG-KD; RM82 and SKNMC cell lines) and ENG-overexpressing (pENG; TC71 cell lines) models were generated by shRNA technology and pDisplay vectors, respectively, and confirmed by qRT-PCR, western blotting and flow cytometry. In vitro MMP14-knockout (MMP14-KO; RM82 and SKNMC) models were generated by CRISPR-Cas9 and confirmed by western blotting and Sanger sequencing. Transwell migration/invasion, adhesion, clonogenicity and proliferation assays were performed in vitro. Actin filament organization was evaluated by immunofluorescence. Extracellular vesicles (EVs) were isolated by ultracentrifugation and density gradient separation. Transcriptomic profiling was performed by Clarion S Human arrays followed by Gene Set Enrichment Analysis. HiPathia tool was used to recode the transcriptomic data into measurements of cell activity by applying mechanistic models. Reverse Phase Protein Array (RPPA) analysis was evaluated on the ENG-KD RM82 model. ENG-targeting immunoprecipitations (IP) from wild type RM82 protein extracts were analyzed by mass spectrometry (MS). Results: The impaired clonogenic potential of ENG-KD RM82 and SKNMC models suggests a role of ENG on the stemness capacity of ES, without affecting the proliferation rate. The reduced migratory and adhesive phenotype of the ENG-KD RM82 model and the transcriptomic profiling of both ENG-KD RM82 and SKNMC cells, suggest a role of ENG in ES cell migration and adhesion. The altered organization of actin filaments in ENG-KD and pENG models could support a role of ENG in actin filament remodeling. The transcriptomic profiling of ENG-KD models and the RPPA results underscore the regulation of FAK signaling by ENG. The IP-MS analysis of ENG partners identifies Integrin-Linked Kinase-Associated serine/threonine Phosphatase (ILKAP) as one of the main interactors of ENG in RM82 cells, suggesting its possible association with the focal adhesion member ILK. ENG is enriched in EVs from different ES cell lines. The transcriptomic profiling of MMP14-KO SKNMC cells highlights the involvement of MMP14 activity in the extracellular matrix organization of ES cells. Conclusion: ENG favors a pro-migratory phenotype in ES cells. These findings help to better understand the molecular landscape of tumoral cells from ES patients, and might have potential clinical implications. Citation Format: Pilar Puerto-Camacho, Ana Teresa Amaral, Juan Diaz-Martin, Alfonso Bolado-Carrancio, Carmen Jordan-Perez, Carmen Salguero-Aranda, Marina Esteban-Medina, Inmaculada Alamo-Alvarez, Joaquin Dopazo, Carmelo Bernabeu, Adam Byron, Valerie G. Brunton, Enrique de Álava. The relevance of endoglin and MMP14 to the metastatic potential of Ewing sarcoma cells [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 6158.</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="115437739"><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="115437739"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437739; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437739]").text(description); $(".js-view-count[data-work-id=115437739]").attr('title', description).tooltip(); 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</script> <div class="js-work-strip profile--work_container" data-work-id="115437738"><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/115437738/Dysregulation_of_transforming_growth_factor_beta_signaling_in_scleroderma_Overexpression_of_endoglin_in_cutaneous_scleroderma_fibroblasts_vol_46_pg_1857_2002_"><img alt="Research paper thumbnail of Dysregulation of transforming growth factor beta signaling in scleroderma - Overexpression of endoglin in cutaneous scleroderma fibroblasts (vol 46, pg 1857, 2002)" class="work-thumbnail" src="https://attachments.academia-assets.com/111844844/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/115437738/Dysregulation_of_transforming_growth_factor_beta_signaling_in_scleroderma_Overexpression_of_endoglin_in_cutaneous_scleroderma_fibroblasts_vol_46_pg_1857_2002_">Dysregulation of transforming growth factor beta signaling in scleroderma - Overexpression of endoglin in cutaneous scleroderma fibroblasts (vol 46, pg 1857, 2002)</a></div><div class="wp-workCard_item"><span>Arthritis & Rheumatism</span><span>, Oct 1, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Alterations in the expression of transforming growth factor-ßl (TGF-ßl) have been implicated for ...</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">Alterations in the expression of transforming growth factor-ßl (TGF-ßl) have been implicated for malignancies of both human and experimental animal models. To further investigate the role of TGF-ßl in chemically-induced esophageal tumorigenesis, the expression of TGF-ßl was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical studies in Af-nitrosomethylbenzylamine (NMBA)-induced rat esophageal tumori genesis. We observed no significant difference in TGF-ßl mRNA levels between 25-week papillomas and normal rat esophageal epithelium. However, TGF-ßl mRNA levels were increased 2.9-fold (p<0.05) in 45-week papillomas induced by NMBA, when compared to normal rat esophageal epithelium. Immunohistochemical studies revealed a decreased intracellular TGF-ßl immunoreactivity in the papillomas when compared to the normal rat esophageal epithelium, indicating the existence of a discordance between TGF-ßl mRNA and protein expression. Furthermore, by immunohistochemical staining of proliferating cell nuclear antigen (PCNA), a predominantely mutually exclusive staining pattern was observed for TGF-ßl and PCNA. These findings suggest that overexpression of TGF-ßl mRNA occurs late in NMBA-induced rat esophageal tumorigenesis, and the discordant mRNA and protein expression may result in tumor evasion from TGF-ßl controlled negative growth regulation, thus promoting tumor progression in this model.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b885ac24ec2fc0d86e39b763de44ccd5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844844,"asset_id":115437738,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844844/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="115437738"><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="115437738"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437738; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "b885ac24ec2fc0d86e39b763de44ccd5" } } $('.js-work-strip[data-work-id=115437738]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437738,"title":"Dysregulation of transforming growth factor beta signaling in scleroderma - Overexpression of endoglin in cutaneous scleroderma fibroblasts (vol 46, pg 1857, 2002)","internal_url":"https://www.academia.edu/115437738/Dysregulation_of_transforming_growth_factor_beta_signaling_in_scleroderma_Overexpression_of_endoglin_in_cutaneous_scleroderma_fibroblasts_vol_46_pg_1857_2002_","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"attachments":[{"id":111844844,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844844/thumbnails/1.jpg","file_name":"ijo.9.3.47320240226-1-9ltvsw.pdf","download_url":"https://www.academia.edu/attachments/111844844/download_file","bulk_download_file_name":"Dysregulation_of_transforming_growth_fac.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844844/ijo.9.3.47320240226-1-9ltvsw-libre.pdf?1708956263=\u0026response-content-disposition=attachment%3B+filename%3DDysregulation_of_transforming_growth_fac.pdf\u0026Expires=1740039264\u0026Signature=dDXQCf5rbwfbGhFmx6HEr6LkGjbEaozO6q1MMU3O6BRJsZ6zufWQnumKQmAe~ANVEtGazwAu01nAUabEEgq-1hrqqIF4SBrhxGOaIjyHLZQPxmbS5FkK377C~P4Oddeynn8tmuu9~R4HAAw7siRQPomIrmnkYNrKrnx-FqhNFrr1NroXRnYdwB8MpIzRd9NDTVTzCnQou4M3wizyJhWbip5mkX~v8LnGWuTaNnlX14H04nUk~AAcifHbyDtDsvCcsV35v-RgzyUDvrkTYjlTOZlgRsV-PfHWofUja9pGd4Ptu4X1CLVAkGxFzvXXZ24tkomKgpKgPYetq1SXk4OeBw__\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="115437736"><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/115437736/Endoglin_a_component_of_the_TGF_%CE%B2_receptor_system_is_a_differentiation_marker_of_human_choriocarcinoma_cells"><img alt="Research paper thumbnail of Endoglin, a component of the TGF-β receptor system, is a differentiation marker of human choriocarcinoma 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/115437736/Endoglin_a_component_of_the_TGF_%CE%B2_receptor_system_is_a_differentiation_marker_of_human_choriocarcinoma_cells">Endoglin, a component of the TGF-β receptor system, is a differentiation marker of human choriocarcinoma cells</a></div><div class="wp-workCard_item"><span>International Journal of Cancer</span><span>, May 18, 1998</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Abstract Endoglin is an integral membrane glycoprotein that binds transforming growth factor-β1 (...</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">Abstract Endoglin is an integral membrane glycoprotein that binds transforming growth factor-β1 (TGF-β1) with high affinity and it is strongly expressed on syncytiotrophoblasts throughout pregnancy. Here, we describe the expression of endoglin by the ...</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="115437736"><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="115437736"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437736; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437736]").text(description); $(".js-view-count[data-work-id=115437736]").attr('title', description).tooltip(); 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</script> <div class="js-work-strip profile--work_container" data-work-id="115437735"><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/115437735/Extracellular_signal_regulated_protein_kinase_signaling_pathway_negatively_regulates_the_phenotypic_and_functional_maturation_of_monocyte_derived_human_dendritic_cells"><img alt="Research paper thumbnail of Extracellular signal–regulated protein kinase signaling pathway negatively regulates the phenotypic and functional maturation of monocyte-derived human dendritic cells" class="work-thumbnail" src="https://attachments.academia-assets.com/111844842/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/115437735/Extracellular_signal_regulated_protein_kinase_signaling_pathway_negatively_regulates_the_phenotypic_and_functional_maturation_of_monocyte_derived_human_dendritic_cells">Extracellular signal–regulated protein kinase signaling pathway negatively regulates the phenotypic and functional maturation of monocyte-derived human dendritic cells</a></div><div class="wp-workCard_item"><span>Blood</span><span>, Oct 1, 2001</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Dendritic cells (DC) are highly specialized antigen-presenting cells that on activation by inflam...</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">Dendritic cells (DC) are highly specialized antigen-presenting cells that on activation by inflammatory stimuli (eg, tumor necrosis factor ␣ [TNF-␣] and interleukin-1␤ [IL-1␤]) or infectious agents (eg, lipopolysaccharide [LPS]), mature and migrate into lymphoid organs. During maturation, DC acquire the capacity to prime and polarize resting naive T lymphocytes. Maturation of monocyte-derived DC (MDDC) is inhibited by the p38 mitogenactivated protein kinase (MAPK) inhibitor SB203580. This study found that in the presence of the mitogen-activated protein kinase kinase 1-extracellular signal-regulated kinase (ERK) inhibitors PD98059 or U0126, TNF-␣-and LPS-induced phenotypic and functional maturation is enhanced. ERK pathway inhibitors increased expression of major histocompatibility complex and costimulatory molecules; loss of mannose-receptor-mediated endocytic activity; nuclear factor-B DNAbinding activity; release of IL-12 p40; and allogeneic T-cell proliferation induced by LPS or TNF-␣. Moreover, PD98059 and U0126 enhanced LPS-triggered production of IL-12 p70. In agreement with the effect of ERK inhibitors, maturation of MDDC was delayed in the presence of serum, an effect that was reversed by U0126. These results indicate that the ERK and p38 MAPK signaling pathways differentially regulate maturation of MDDC and suggest that their relative levels of activation might modulate the initial commitment of naive T-helper (Th) cells toward Th1 or Th2 subsets. The findings also suggest that maturation of MDDC might be pharmacologically modified by altering the relative levels of activation of both intracellular signaling routes. (Blood.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="81d701ba1ffd23ee1d610dbcaaaefaba" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844842,"asset_id":115437735,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844842/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="115437735"><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="115437735"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437735; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437735]").text(description); $(".js-view-count[data-work-id=115437735]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437735; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437735']"); 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: "81d701ba1ffd23ee1d610dbcaaaefaba" } } $('.js-work-strip[data-work-id=115437735]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437735,"title":"Extracellular signal–regulated protein kinase signaling pathway negatively regulates the phenotypic and functional maturation of monocyte-derived human dendritic cells","internal_url":"https://www.academia.edu/115437735/Extracellular_signal_regulated_protein_kinase_signaling_pathway_negatively_regulates_the_phenotypic_and_functional_maturation_of_monocyte_derived_human_dendritic_cells","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"attachments":[{"id":111844842,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844842/thumbnails/1.jpg","file_name":"h8190102175.pdf","download_url":"https://www.academia.edu/attachments/111844842/download_file","bulk_download_file_name":"Extracellular_signal_regulated_protein_k.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844842/h8190102175-libre.pdf?1708956265=\u0026response-content-disposition=attachment%3B+filename%3DExtracellular_signal_regulated_protein_k.pdf\u0026Expires=1740039264\u0026Signature=NI4u5X57MGvoRHAGu-1gqCENoc2gwiArmYoavfQAGCUqyXX1Gyrl9IcEATAg4qe~nN62Z2vmQhj4uZ8vXDL06kHXte5vjchy6SEnIEEkqKD6Ur-GtY9qEal53ka1QxWvcdowTBbWfqh1nCuxbbDOP7W2EbyspfD4qCJ5SyWV4yhTdyTLiGvlL7zDBPFJVtElOAu97s8eQIg9tPREJyAi3PHQyEvBXTM~PsKvLj2nJcktQkL6GDGH8a-c9ns2wkq8Z2K5OFdT45Vuk2mgaaz6H6PaJvk6dsuZa4KBu1nHeB9fvvrkMP7-zqixVgbM6u3qlw-N3itDD62aD-xOumCDcw__\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="115437734"><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/115437734/CD105_inhibits_transforming_growth_factor_beta_Smad3_signalling"><img alt="Research paper thumbnail of CD105 inhibits transforming growth factor-beta-Smad3 signalling" 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/115437734/CD105_inhibits_transforming_growth_factor_beta_Smad3_signalling">CD105 inhibits transforming growth factor-beta-Smad3 signalling</a></div><div class="wp-workCard_item"><span>PubMed</span><span>, Jul 28, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">CD105 (endoglin) is an important component of the transforming growth factor-beta (TGF-beta) rece...</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">CD105 (endoglin) is an important component of the transforming growth factor-beta (TGF-beta) receptor complex and is highly expressed in endothelial cells in tissues undergoing angiogenesis such as healing wounds, infarcts and in a wide range of tumours. In an attempt to understand the molecular mechanism by which CD105 exerts its effects on angiogenesis by modulating TGF-beta1 signalling, in this preliminary communication, CD105 transfected rat myoblasts were utilized as an in vitro model. Overexpression of CD105 in these transfectants antagonised TGF-beta1-mediated inhibition of cell proliferation and reduced TGF-beta1-mediated p3TP-Lux (PAI-1 promoter) luciferase activity. It also reduced (CAGA)12-Luc luciferase activity in response to TGF-beta1. The CAGA sequence is specific for Smad3/4 binding, implying that CD105 is involved in inhibition of TGF-beta1/Smad3 signalling. Furthermore, CD105 overexpression reduced serine phosphorylation of Smad3 and inhibited subsequent nuclear translocation of Smad3. CD105 resulted in high phosphorylation of JNK1, which is able to activate c-Jun. c-Jun is known to inhibit Smad3 transcriptional activity on CAGA sites, suggesting that CD105 may also inhibit Smad3 signalling through JNK1.</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="115437734"><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="115437734"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437734; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437734]").text(description); $(".js-view-count[data-work-id=115437734]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437734; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437734']"); 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" } } $('.js-work-strip[data-work-id=115437734]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437734,"title":"CD105 inhibits transforming growth factor-beta-Smad3 signalling","internal_url":"https://www.academia.edu/115437734/CD105_inhibits_transforming_growth_factor_beta_Smad3_signalling","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"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="115437733"><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/115437733/Homozygous_i_GDF2_i_nonsense_mutations_result_in_a_loss_of_circulating_BMP9_and_BMP10_and_are_associated_with_either_PAH_or_an_HHT_like_syndrome_in_children"><img alt="Research paper thumbnail of Homozygous <i>GDF2</i> nonsense mutations result in a loss of circulating BMP9 and BMP10 and are associated with either PAH or an “HHT‐like” syndrome in children" class="work-thumbnail" src="https://attachments.academia-assets.com/111844838/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/115437733/Homozygous_i_GDF2_i_nonsense_mutations_result_in_a_loss_of_circulating_BMP9_and_BMP10_and_are_associated_with_either_PAH_or_an_HHT_like_syndrome_in_children">Homozygous <i>GDF2</i> nonsense mutations result in a loss of circulating BMP9 and BMP10 and are associated with either PAH or an “HHT‐like” syndrome in children</a></div><div class="wp-workCard_item"><span>Molecular Genetics & Genomic Medicine</span><span>, Apr 9, 2021</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">This is an open access article under the terms of the Creative Commons Attribution License, which...</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">This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1268870917713eb78bfc8b853f81a069" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844838,"asset_id":115437733,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844838/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="115437733"><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="115437733"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437733; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437733]").text(description); $(".js-view-count[data-work-id=115437733]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437733; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437733']"); 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: "1268870917713eb78bfc8b853f81a069" } } $('.js-work-strip[data-work-id=115437733]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437733,"title":"Homozygous \u003ci\u003eGDF2\u003c/i\u003e nonsense mutations result in a loss of circulating BMP9 and BMP10 and are associated with either PAH or an “HHT‐like” syndrome in children","internal_url":"https://www.academia.edu/115437733/Homozygous_i_GDF2_i_nonsense_mutations_result_in_a_loss_of_circulating_BMP9_and_BMP10_and_are_associated_with_either_PAH_or_an_HHT_like_syndrome_in_children","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"attachments":[{"id":111844838,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844838/thumbnails/1.jpg","file_name":"mggm_Hodgson_2021.pdf","download_url":"https://www.academia.edu/attachments/111844838/download_file","bulk_download_file_name":"Homozygous_i_GDF2_i_nonsense_mutations_r.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844838/mggm_Hodgson_2021-libre.pdf?1708956268=\u0026response-content-disposition=attachment%3B+filename%3DHomozygous_i_GDF2_i_nonsense_mutations_r.pdf\u0026Expires=1740039264\u0026Signature=MU7r5AMlg-7-4Ou0~YVYGZWFvte9NgaIXsLO36TPUbDuQ2GV90RyMDSYKBf0rwnWJhzYgNi5TI5OXvFbOQneLoXVUoN-MKyzUzOhP-hCIPg9TSyItBWCECasDPl1PVio~EzNiTK9Cc8pzn0VreY0Az7k-Nlb4qXeVegAkMHTdYw3WbkC0~vNQQ42F8gnsU01WYtn-KOlgsDDNUzSKBW71480oCCK~V1I2aUfnLLppz4uPzKWrLMmH3nakUfwjoo2u4ONMGTJ2eyzpw~P8s8L~zEOcQlJ1uCMyYOkEVfjzMBta1TuR43QOqvqApcikkADuWgTx4D6EVEE6vpftuNp~g__\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="115437732"><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/115437732/Correlation_Between_Endoglin_and_Malignant_Phenotype_in_Human_Melanoma_Cells_Analysis_of_hsa_mir_214_and_hsa_mir_370_in_Cells_and_Their_Extracellular_Vesicles"><img alt="Research paper thumbnail of Correlation Between Endoglin and Malignant Phenotype in Human Melanoma Cells: Analysis of hsa-mir-214 and hsa-mir-370 in Cells and Their Extracellular Vesicles" class="work-thumbnail" src="https://attachments.academia-assets.com/111844804/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/115437732/Correlation_Between_Endoglin_and_Malignant_Phenotype_in_Human_Melanoma_Cells_Analysis_of_hsa_mir_214_and_hsa_mir_370_in_Cells_and_Their_Extracellular_Vesicles">Correlation Between Endoglin and Malignant Phenotype in Human Melanoma Cells: Analysis of hsa-mir-214 and hsa-mir-370 in Cells and Their Extracellular Vesicles</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Endoglin (CD105) is an auxiliary receptor of transforming growth factor (TGF)-b family members th...</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">Endoglin (CD105) is an auxiliary receptor of transforming growth factor (TGF)-b family members that is expressed in human melanomas. It is heterogeneously expressed by primary and metastatic melanoma cells, and endoglin targeting as a therapeutic strategy for melanoma tumors is currently been explored. However, its involvement in tumor development and malignancy is not fully understood. Here, we find that endoglin expression correlates with malignancy of primary melanomas and cultured melanoma cell lines. Next, we have analyzed the effect of ectopic endoglin expression on two miRNAs (hsa-mir-214 and hsa-mir-370), both involved in melanoma tumor progression and endoglin regulation. We show that compared with control cells, overexpression of endoglin in the WM-164 melanoma cell line induces; (i) a significant increase of hsa-mir-214 levels in small extracellular vesicles (EVs) as well as an increased trend in cells; and (ii) significantly lower levels of hsa-mir-370 in the EVs fractions, whereas no significant differences were found in cells. As hsa-mir-214 and hsa-mir-370 are not just involved in melanoma tumor progression, but they can also target endoglin-expressing endothelial cells in the tumor vasculature, these results suggest a complex and differential regulatory mechanism involving the intracellular and extracellular signaling of</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="8232fb8408a3b008e5089c3c2c3f7cad" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844804,"asset_id":115437732,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844804/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="115437732"><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="115437732"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437732; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437732]").text(description); $(".js-view-count[data-work-id=115437732]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437732; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437732']"); 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: "8232fb8408a3b008e5089c3c2c3f7cad" } } $('.js-work-strip[data-work-id=115437732]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437732,"title":"Correlation Between Endoglin and Malignant Phenotype in Human Melanoma Cells: Analysis of hsa-mir-214 and hsa-mir-370 in Cells and Their Extracellular Vesicles","internal_url":"https://www.academia.edu/115437732/Correlation_Between_Endoglin_and_Malignant_Phenotype_in_Human_Melanoma_Cells_Analysis_of_hsa_mir_214_and_hsa_mir_370_in_Cells_and_Their_Extracellular_Vesicles","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"attachments":[{"id":111844804,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844804/thumbnails/1.jpg","file_name":"978-3-031-26163-3_14.pdf","download_url":"https://www.academia.edu/attachments/111844804/download_file","bulk_download_file_name":"Correlation_Between_Endoglin_and_Maligna.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844804/978-3-031-26163-3_14-libre.pdf?1708956273=\u0026response-content-disposition=attachment%3B+filename%3DCorrelation_Between_Endoglin_and_Maligna.pdf\u0026Expires=1740039264\u0026Signature=dFJ~XjO0ofqsHLIsQF5XT3UF1CvBFZ5F7qEavJzWmqjQT-YdV~k-SpFCgvoqbE7UIBQ-PhIUJNjW6z0ydClD87C8RXCdQx-4Bz4bxbsgtqliCTu28vucuT3XcqFaHENF7C53mCVN87tmr1H2Vu3TOICSGNeURVqsLU1r~Z3qRzp4Thw1UxUXZLP8BeZwiEfVpyj-oQbIeDtOPYoBOv9gu6otXo7CiinhMIdX44TNC1SaBEdyTo0sXdv6ULANeG~Cy7KP8AUmsRxSxEvbFa9136kzkRYgTC0Rnle-pkpEfusgEPet6sJFPS3K8x9TcGKWqbwrDtuPH4N6v2ng-KeCng__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":111844805,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844805/thumbnails/1.jpg","file_name":"978-3-031-26163-3_14.pdf","download_url":"https://www.academia.edu/attachments/111844805/download_file","bulk_download_file_name":"Correlation_Between_Endoglin_and_Maligna.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844805/978-3-031-26163-3_14-libre.pdf?1708956267=\u0026response-content-disposition=attachment%3B+filename%3DCorrelation_Between_Endoglin_and_Maligna.pdf\u0026Expires=1740039264\u0026Signature=W-9wDSGCYXAWAOT2eYEjW2jw~McahABtF7WH6xSYuQOIKitkdrmOXEJVvRzE8cSO3MHPfVP90OJLnU7xY2~TuVkZ7xcSTIDMIvMY9paQ~JGIKQPnrs-9Nx5EYAbnXWc-sE3bYLgPkTwlvLj8Sib-rag602ntS1BE9DkyFxwNJj9JzefoShr~-yxvPZRcOSGNLmuJgn7E0vF-ageaSWuRkAfjzwd4C8oON6ApTUJNJf0RQDelze84K8lfcfA7Ut4-kwBpXI5kROmlPgbMFyLrLFcWVy3FQ985x3vxKIo3gRLsOShXDAVv72-a9BSPh4geu3hbzEweWQh8rNuuHlQewg__\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="115437730"><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/115437730/TGF_%CE%B2_Signalling_and_Its_Role_in_Cancer_Progression_and_Metastasis"><img alt="Research paper thumbnail of TGF-β Signalling and Its Role in Cancer Progression and Metastasis" class="work-thumbnail" src="https://attachments.academia-assets.com/111844840/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/115437730/TGF_%CE%B2_Signalling_and_Its_Role_in_Cancer_Progression_and_Metastasis">TGF-β Signalling and Its Role in Cancer Progression and Metastasis</a></div><div class="wp-workCard_item"><span>eLS</span><span>, Aug 16, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The transforming growth factor-β (TGF-β) system signals via protein kinase receptors and SMAD med...</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 transforming growth factor-β (TGF-β) system signals via protein kinase receptors and SMAD mediators to regulate a large number of biological processes. Alterations of the TGF-β signalling pathway are implicated in human cancer. Prior to tumour initiation and early during progression, TGF-β acts as a tumour suppressor; however, at later stages, it is often a tumour promoter. Knowledge about the mechanisms involved in TGF-β signal transduction has allowed a better understanding of cancer progression, invasion, metastasis and epithelial-to-mesenchymal transition. Furthermore, several molecular targets with great potential in therapeutic interventions have been identified. This review discusses the TGF-β signalling pathway, its involvement in cancer and current therapeutic approaches.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="287a2ab438714898c496aac9aaff735f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844840,"asset_id":115437730,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844840/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="115437730"><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="115437730"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437730; 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As expression of major histocompatibility (MHC) antigens is a prerequisite for organ specific autoimmunity, the expression of HLA class I (P2-micro</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0004b386c3233f9b9193b966214b7430" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844841,"asset_id":115437729,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844841/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="115437729"><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="115437729"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437729; 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They a r e a l t e r e d i n tufA and tufis, the two genes coding f o r the elongation f a c t o r EF-Tu. One of these genes can be i n a c t i v a t e d by i n s e r t i o n of bacteriophage Mu. This enabled us t o study t h e nature and funct i o n o f t h e mutant EF-Tu s p e c i e s (c. f. a l s o F. 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</script> <div class="js-work-strip profile--work_container" data-work-id="115437724"><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/115437724/Endoglin_and_MMP14_Contribute_to_Ewing_Sarcoma_Spreading_by_Modulation_of_Cell_Matrix_Interactions"><img alt="Research paper thumbnail of Endoglin and MMP14 Contribute to Ewing Sarcoma Spreading by Modulation of Cell–Matrix Interactions" class="work-thumbnail" src="https://attachments.academia-assets.com/111844802/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" rel="nofollow" href="https://www.academia.edu/115437724/Endoglin_and_MMP14_Contribute_to_Ewing_Sarcoma_Spreading_by_Modulation_of_Cell_Matrix_Interactions">Endoglin and MMP14 Contribute to Ewing Sarcoma Spreading by Modulation of Cell–Matrix Interactions</a></div><div class="wp-workCard_item"><span>International Journal of Molecular Sciences</span><span>, Aug 4, 2022</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="196909ec53d7f602dc682756d1cef037" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844802,"asset_id":115437724,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844802/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="115437724"><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="115437724"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437724; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="115437723"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/115437723/Editorial_Role_of_membrane_bound_and_circulating_endoglin_in_disease"><img alt="Research paper thumbnail of Editorial: Role of membrane-bound and circulating endoglin in disease" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/115437723/Editorial_Role_of_membrane_bound_and_circulating_endoglin_in_disease">Editorial: Role of membrane-bound and circulating endoglin in disease</a></div><div class="wp-workCard_item"><span>Frontiers in Medicine</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="115437723"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="115437723"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437723; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437723]").text(description); $(".js-view-count[data-work-id=115437723]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437723; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437723']"); 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" } } $('.js-work-strip[data-work-id=115437723]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437723,"title":"Editorial: Role of membrane-bound and circulating endoglin in disease","internal_url":"https://www.academia.edu/115437723/Editorial_Role_of_membrane_bound_and_circulating_endoglin_in_disease","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"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="115437722"><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/115437722/Monoclonal_anti_endoglin_antibody_TRC105_carotuximab_prevents_hypercholesterolemia_and_hyperglycemia_induced_endothelial_dysfunction_in_human_aortic_endothelial_cells"><img alt="Research paper thumbnail of Monoclonal anti-endoglin antibody TRC105 (carotuximab) prevents hypercholesterolemia and hyperglycemia-induced endothelial dysfunction in human aortic endothelial cells" class="work-thumbnail" src="https://attachments.academia-assets.com/111844843/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/115437722/Monoclonal_anti_endoglin_antibody_TRC105_carotuximab_prevents_hypercholesterolemia_and_hyperglycemia_induced_endothelial_dysfunction_in_human_aortic_endothelial_cells">Monoclonal anti-endoglin antibody TRC105 (carotuximab) prevents hypercholesterolemia and hyperglycemia-induced endothelial dysfunction in human aortic endothelial cells</a></div><div class="wp-workCard_item"><span>Frontiers in Medicine</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Endoglin (Eng) is a co-receptor of the transforming growth factor β superfamily playing an import...</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">Endoglin (Eng) is a co-receptor of the transforming growth factor β superfamily playing an important role in endothelial dysfunction. TRC105 (carotuximab) is a monoclonal antibody that blocks Eng and its downstream Smad signaling pathway. Here we have investigated for the first time the effects of TRC105 treatment on the development of endothelial dysfunction induced by 7-ketocholesterol (7K) or high glucose (HG), focusing on Eng expression, signaling, and function. In the hypercholesterolemia study, human aortic endothelial cells (HAoECs) were treated with TRC105 (300 μg/ml) for 1 h, followed by the addition of 7K (10 μg/ml) for another 12 h. In the hyperglycemia study, HAoECs were exposed to HG (45 mM) for 60 h, followed by the addition of TRC105 for another 12 h, and cells treated with 5mM glucose and 40 mM mannitol served as control. Protein levels, adhesion, and transmigration of monocytes were assessed by flow cytometry, mRNA expression was measured by qRT-PCR. 7K and HG treat...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="cb69a7ad6276d29671d7926e61e36d30" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844843,"asset_id":115437722,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844843/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="115437722"><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="115437722"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437722; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="115437721"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/115437721/Novel_vascular_roles_of_human_endoglin_in_pathophysiology"><img alt="Research paper thumbnail of Novel vascular roles of human endoglin in pathophysiology" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/115437721/Novel_vascular_roles_of_human_endoglin_in_pathophysiology">Novel vascular roles of human endoglin in pathophysiology</a></div><div class="wp-workCard_item"><span>Journal of Thrombosis and Haemostasis</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="115437721"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="115437721"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437721; 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window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437719]").text(description); $(".js-view-count[data-work-id=115437719]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437719; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437719']"); 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: "4dbf24569f5214ae6c808f04ab203304" } } $('.js-work-strip[data-work-id=115437719]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437719,"title":"Emerging role of endothelial endoglin in integrin-mediated cell adhesion","internal_url":"https://www.academia.edu/115437719/Emerging_role_of_endothelial_endoglin_in_integrin_mediated_cell_adhesion","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"attachments":[{"id":111844836,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844836/thumbnails/1.jpg","file_name":"jmm2017.pdf","download_url":"https://www.academia.edu/attachments/111844836/download_file","bulk_download_file_name":"Emerging_role_of_endothelial_endoglin_in.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844836/jmm2017-libre.pdf?1708956260=\u0026response-content-disposition=attachment%3B+filename%3DEmerging_role_of_endothelial_endoglin_in.pdf\u0026Expires=1740039264\u0026Signature=B~ydaUSfuv7IyAm5O4vfGJKZ9cBwB~Cy6pVCSoIZo3RPz2p-zj1fsNSCLCCZxMd4Hj6xJJteYRANq9xZjD9BsffYtWXpVCgczUWC6qsPrKWXEOHOFuxiZjUvS3aeGIzjOZGmX3-qXbWpwXw-eJuZcGxhBS~2PAm6InIrA~R84lbURdSkyFdA~gvwX0XeFyqMhe4O6IMRSqAPkefJ8yWVaxAV0LEl5wgsYVTukqHwHVKUI~V32aU1Es2UYkrhoObm4rGL~J~B05QhSrNj6l4rzmahUZZvSF-swHRVKjUiMa8W5qJ0TtZYty-1aHPORiujCE8R6-iqSx0hGT2-59nIpQ__\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="115437718"><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/115437718/The_Tgf_%CE%B2_Bmp_Co_Receptor_Endoglin_Is_a_Key_Component_of_the_Molecular_Oscillator_That_Regulates_the_Hair_Follicle_Cycle"><img alt="Research paper thumbnail of The Tgf-β/Bmp Co-Receptor Endoglin Is a Key Component of the Molecular Oscillator That Regulates the Hair Follicle Cycle" class="work-thumbnail" src="https://attachments.academia-assets.com/111844991/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/115437718/The_Tgf_%CE%B2_Bmp_Co_Receptor_Endoglin_Is_a_Key_Component_of_the_Molecular_Oscillator_That_Regulates_the_Hair_Follicle_Cycle">The Tgf-β/Bmp Co-Receptor Endoglin Is a Key Component of the Molecular Oscillator That Regulates the Hair Follicle Cycle</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The hair follicle is a biological oscillator that alternates growth, regression, and rest phases ...</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 hair follicle is a biological oscillator that alternates growth, regression, and rest phases driven by the sequential activation of the proliferation/differentiation programs of resident stem cell populations. The activation of hair follicle stem cell niches and subsequent entry into the growing phase is mainly regulated by Wnt/β-catenin signalling, while regression and resting phases are mainly regulated by Tgf-β/Bmp/Smad activity. A major question still unresolved is the nature of the molecular switch that dictates the coordinated transition between both signalling pathways. Here we have focused on the role of Endoglin (Eng), a key co-receptor for members of the Tgfβ/Bmp family of growth factors. Using an Eng haploinsufficient mouse model, we report that Eng is required to maintain a correct follicle cycling pattern and for an adequate stimulation of hair follicle stem cell niches. We further report that β-catenin binds to the Eng promoter depending on Bmp signalling. Moreover, we show that β-catenin interacts with Smad4 in a Bmp/Eng-dependent context and both proteins act synergistically to activate Eng promoter transcription. These observations point to the existence of a growth/rest switching mechanism in the hair follicle that is based on an Eng-dependent feedback cross-talk between Wnt/β-catenin and Bmp/Smad signals.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="769b17ac2ba07345f196e82cf25c083f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844991,"asset_id":115437718,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844991/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="115437718"><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="115437718"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437718; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437718]").text(description); $(".js-view-count[data-work-id=115437718]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437718; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437718']"); 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: "769b17ac2ba07345f196e82cf25c083f" } } $('.js-work-strip[data-work-id=115437718]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437718,"title":"The Tgf-β/Bmp Co-Receptor Endoglin Is a Key Component of the Molecular Oscillator That Regulates the Hair Follicle Cycle","internal_url":"https://www.academia.edu/115437718/The_Tgf_%CE%B2_Bmp_Co_Receptor_Endoglin_Is_a_Key_Component_of_the_Molecular_Oscillator_That_Regulates_the_Hair_Follicle_Cycle","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"attachments":[{"id":111844991,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844991/thumbnails/1.jpg","file_name":"2019_Calvo_Sanchez_JMCB_11_39_Eng_hair.pdf","download_url":"https://www.academia.edu/attachments/111844991/download_file","bulk_download_file_name":"The_Tgf__Bmp_Co_Receptor_Endoglin_Is_a.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844991/2019_Calvo_Sanchez_JMCB_11_39_Eng_hair-libre.pdf?1708956267=\u0026response-content-disposition=attachment%3B+filename%3DThe_Tgf__Bmp_Co_Receptor_Endoglin_Is_a.pdf\u0026Expires=1740039264\u0026Signature=HZIv55E3PQf2ozkOkiJeiH5vkzI8gjm-dfbmS2oRYiwMXLtwRuWYI~1pwQu3jSHZhvt0MjQ3T7d0gLFzgpF76MV5cif962Fw~xZ6YwRt9kYivuYU0QfabOpuN44i4s8MlwYuUdER0W5xHbIeQj2AP4kjl-YJIIGPoLbn59G46Hg5r5SQa6kxDTNMpAVlsqwUfBakV-Ix9Kl-41ZrJ95dV~qjYosmo-6XeQaEwwdy40Q815OmLlA7BZPmYqgaJNB82YL5nreDw-9F2XZrl5otuWOH8NxgF94QE3oISjNZb21Y~cdATUSX6Kr0qrowoRFaV~UA~izHIVQcAR9SbIJ7bg__\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="115437717"><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/115437717/Mapping_the_Ribosomal_Exit_Site_of_the_Nascent_Polypeptide_Chain_by_Immune_Electron_Microscopy"><img alt="Research paper thumbnail of Mapping the Ribosomal Exit Site of the Nascent Polypeptide Chain by Immune Electron Microscopy" 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/115437717/Mapping_the_Ribosomal_Exit_Site_of_the_Nascent_Polypeptide_Chain_by_Immune_Electron_Microscopy">Mapping the Ribosomal Exit Site of the Nascent Polypeptide Chain by Immune Electron Microscopy</a></div><div class="wp-workCard_item"><span>Proceedings, annual meeting, Electron Microscopy Society of America</span><span>, 1981</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Immune electron microscopy is providing information on the three dimensional locations of many fu...</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">Immune electron microscopy is providing information on the three dimensional locations of many functional sites on the ribosome. In particular, localization of the exit site of the newly synthesized protein chain is expected to provide information on the mechanisms of protein synthesis and on the nature of the ribosome-membrane association. Theoretically the nascent chains of the largest proteins could be visible as they leave the ribosome, but in practice they have not been observed. In order to map their exit site we have made antibodies against one particular enzyme and then applied immune electron microscopy to a polysome fraction enriched for that special protein.In a mutant of Escherichia coli constitutive for the enzyme beta-galac- tosidase, this enzyme accounts for approximately 25% of the total protein (1). Because of the high molecular weight of beta-galactosidase, a fraction of larger polysomes, further enriched in this emzyme, was obtained by differential centrifugation....</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="115437717"><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="115437717"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437717; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437717]").text(description); $(".js-view-count[data-work-id=115437717]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437717; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437717']"); 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); 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Although the outcome of ES patients bearing primary tumors has improved significantly, patients with metastatic ES still have a poor prognosis. The MSC marker endoglin/CD105 (ENG) and the ENG-shedding protease MMP14 have been, respectively, described as cell migration and invasion regulators. In our attempt to better understand the mechanism of ES progression, we are focusing on the role of ENG and MMP14 in ES cells. Methods: In vitro ENG-knockdown (ENG-KD; RM82 and SKNMC cell lines) and ENG-overexpressing (pENG; TC71 cell lines) models were generated by shRNA technology and pDisplay vectors, respectively, and confirmed by qRT-PCR, western blotting and flow cytometry. In vitro MMP14-knockout (MMP14-KO; RM82 and SKNMC) models were generated by CRISPR-Cas9 and confirmed by western blotting and Sanger sequencing. Transwell migration/invasion, adhesion, clonogenicity and proliferation assays were performed in vitro. Actin filament organization was evaluated by immunofluorescence. Extracellular vesicles (EVs) were isolated by ultracentrifugation and density gradient separation. Transcriptomic profiling was performed by Clarion S Human arrays followed by Gene Set Enrichment Analysis. HiPathia tool was used to recode the transcriptomic data into measurements of cell activity by applying mechanistic models. Reverse Phase Protein Array (RPPA) analysis was evaluated on the ENG-KD RM82 model. ENG-targeting immunoprecipitations (IP) from wild type RM82 protein extracts were analyzed by mass spectrometry (MS). Results: The impaired clonogenic potential of ENG-KD RM82 and SKNMC models suggests a role of ENG on the stemness capacity of ES, without affecting the proliferation rate. The reduced migratory and adhesive phenotype of the ENG-KD RM82 model and the transcriptomic profiling of both ENG-KD RM82 and SKNMC cells, suggest a role of ENG in ES cell migration and adhesion. The altered organization of actin filaments in ENG-KD and pENG models could support a role of ENG in actin filament remodeling. The transcriptomic profiling of ENG-KD models and the RPPA results underscore the regulation of FAK signaling by ENG. The IP-MS analysis of ENG partners identifies Integrin-Linked Kinase-Associated serine/threonine Phosphatase (ILKAP) as one of the main interactors of ENG in RM82 cells, suggesting its possible association with the focal adhesion member ILK. ENG is enriched in EVs from different ES cell lines. The transcriptomic profiling of MMP14-KO SKNMC cells highlights the involvement of MMP14 activity in the extracellular matrix organization of ES cells. Conclusion: ENG favors a pro-migratory phenotype in ES cells. These findings help to better understand the molecular landscape of tumoral cells from ES patients, and might have potential clinical implications. Citation Format: Pilar Puerto-Camacho, Ana Teresa Amaral, Juan Diaz-Martin, Alfonso Bolado-Carrancio, Carmen Jordan-Perez, Carmen Salguero-Aranda, Marina Esteban-Medina, Inmaculada Alamo-Alvarez, Joaquin Dopazo, Carmelo Bernabeu, Adam Byron, Valerie G. Brunton, Enrique de Álava. The relevance of endoglin and MMP14 to the metastatic potential of Ewing sarcoma cells [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 6158.</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="115437739"><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="115437739"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437739; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437739]").text(description); $(".js-view-count[data-work-id=115437739]").attr('title', description).tooltip(); 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</script> <div class="js-work-strip profile--work_container" data-work-id="115437738"><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/115437738/Dysregulation_of_transforming_growth_factor_beta_signaling_in_scleroderma_Overexpression_of_endoglin_in_cutaneous_scleroderma_fibroblasts_vol_46_pg_1857_2002_"><img alt="Research paper thumbnail of Dysregulation of transforming growth factor beta signaling in scleroderma - Overexpression of endoglin in cutaneous scleroderma fibroblasts (vol 46, pg 1857, 2002)" class="work-thumbnail" src="https://attachments.academia-assets.com/111844844/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/115437738/Dysregulation_of_transforming_growth_factor_beta_signaling_in_scleroderma_Overexpression_of_endoglin_in_cutaneous_scleroderma_fibroblasts_vol_46_pg_1857_2002_">Dysregulation of transforming growth factor beta signaling in scleroderma - Overexpression of endoglin in cutaneous scleroderma fibroblasts (vol 46, pg 1857, 2002)</a></div><div class="wp-workCard_item"><span>Arthritis & Rheumatism</span><span>, Oct 1, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Alterations in the expression of transforming growth factor-ßl (TGF-ßl) have been implicated for ...</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">Alterations in the expression of transforming growth factor-ßl (TGF-ßl) have been implicated for malignancies of both human and experimental animal models. To further investigate the role of TGF-ßl in chemically-induced esophageal tumorigenesis, the expression of TGF-ßl was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical studies in Af-nitrosomethylbenzylamine (NMBA)-induced rat esophageal tumori genesis. We observed no significant difference in TGF-ßl mRNA levels between 25-week papillomas and normal rat esophageal epithelium. However, TGF-ßl mRNA levels were increased 2.9-fold (p<0.05) in 45-week papillomas induced by NMBA, when compared to normal rat esophageal epithelium. Immunohistochemical studies revealed a decreased intracellular TGF-ßl immunoreactivity in the papillomas when compared to the normal rat esophageal epithelium, indicating the existence of a discordance between TGF-ßl mRNA and protein expression. Furthermore, by immunohistochemical staining of proliferating cell nuclear antigen (PCNA), a predominantely mutually exclusive staining pattern was observed for TGF-ßl and PCNA. These findings suggest that overexpression of TGF-ßl mRNA occurs late in NMBA-induced rat esophageal tumorigenesis, and the discordant mRNA and protein expression may result in tumor evasion from TGF-ßl controlled negative growth regulation, thus promoting tumor progression in this model.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b885ac24ec2fc0d86e39b763de44ccd5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844844,"asset_id":115437738,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844844/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="115437738"><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="115437738"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437738; 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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="115437736"><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/115437736/Endoglin_a_component_of_the_TGF_%CE%B2_receptor_system_is_a_differentiation_marker_of_human_choriocarcinoma_cells"><img alt="Research paper thumbnail of Endoglin, a component of the TGF-β receptor system, is a differentiation marker of human choriocarcinoma 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/115437736/Endoglin_a_component_of_the_TGF_%CE%B2_receptor_system_is_a_differentiation_marker_of_human_choriocarcinoma_cells">Endoglin, a component of the TGF-β receptor system, is a differentiation marker of human choriocarcinoma cells</a></div><div class="wp-workCard_item"><span>International Journal of Cancer</span><span>, May 18, 1998</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Abstract Endoglin is an integral membrane glycoprotein that binds transforming growth factor-β1 (...</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">Abstract Endoglin is an integral membrane glycoprotein that binds transforming growth factor-β1 (TGF-β1) with high affinity and it is strongly expressed on syncytiotrophoblasts throughout pregnancy. Here, we describe the expression of endoglin by the ...</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="115437736"><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="115437736"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437736; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437736]").text(description); $(".js-view-count[data-work-id=115437736]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437736; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437736']"); 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); 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</script> <div class="js-work-strip profile--work_container" data-work-id="115437735"><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/115437735/Extracellular_signal_regulated_protein_kinase_signaling_pathway_negatively_regulates_the_phenotypic_and_functional_maturation_of_monocyte_derived_human_dendritic_cells"><img alt="Research paper thumbnail of Extracellular signal–regulated protein kinase signaling pathway negatively regulates the phenotypic and functional maturation of monocyte-derived human dendritic cells" class="work-thumbnail" src="https://attachments.academia-assets.com/111844842/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/115437735/Extracellular_signal_regulated_protein_kinase_signaling_pathway_negatively_regulates_the_phenotypic_and_functional_maturation_of_monocyte_derived_human_dendritic_cells">Extracellular signal–regulated protein kinase signaling pathway negatively regulates the phenotypic and functional maturation of monocyte-derived human dendritic cells</a></div><div class="wp-workCard_item"><span>Blood</span><span>, Oct 1, 2001</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Dendritic cells (DC) are highly specialized antigen-presenting cells that on activation by inflam...</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">Dendritic cells (DC) are highly specialized antigen-presenting cells that on activation by inflammatory stimuli (eg, tumor necrosis factor ␣ [TNF-␣] and interleukin-1␤ [IL-1␤]) or infectious agents (eg, lipopolysaccharide [LPS]), mature and migrate into lymphoid organs. During maturation, DC acquire the capacity to prime and polarize resting naive T lymphocytes. Maturation of monocyte-derived DC (MDDC) is inhibited by the p38 mitogenactivated protein kinase (MAPK) inhibitor SB203580. This study found that in the presence of the mitogen-activated protein kinase kinase 1-extracellular signal-regulated kinase (ERK) inhibitors PD98059 or U0126, TNF-␣-and LPS-induced phenotypic and functional maturation is enhanced. ERK pathway inhibitors increased expression of major histocompatibility complex and costimulatory molecules; loss of mannose-receptor-mediated endocytic activity; nuclear factor-B DNAbinding activity; release of IL-12 p40; and allogeneic T-cell proliferation induced by LPS or TNF-␣. Moreover, PD98059 and U0126 enhanced LPS-triggered production of IL-12 p70. In agreement with the effect of ERK inhibitors, maturation of MDDC was delayed in the presence of serum, an effect that was reversed by U0126. These results indicate that the ERK and p38 MAPK signaling pathways differentially regulate maturation of MDDC and suggest that their relative levels of activation might modulate the initial commitment of naive T-helper (Th) cells toward Th1 or Th2 subsets. The findings also suggest that maturation of MDDC might be pharmacologically modified by altering the relative levels of activation of both intracellular signaling routes. (Blood.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="81d701ba1ffd23ee1d610dbcaaaefaba" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844842,"asset_id":115437735,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844842/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="115437735"><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="115437735"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437735; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437735]").text(description); $(".js-view-count[data-work-id=115437735]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437735; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437735']"); 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: "81d701ba1ffd23ee1d610dbcaaaefaba" } } $('.js-work-strip[data-work-id=115437735]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437735,"title":"Extracellular signal–regulated protein kinase signaling pathway negatively regulates the phenotypic and functional maturation of monocyte-derived human dendritic cells","internal_url":"https://www.academia.edu/115437735/Extracellular_signal_regulated_protein_kinase_signaling_pathway_negatively_regulates_the_phenotypic_and_functional_maturation_of_monocyte_derived_human_dendritic_cells","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"attachments":[{"id":111844842,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844842/thumbnails/1.jpg","file_name":"h8190102175.pdf","download_url":"https://www.academia.edu/attachments/111844842/download_file","bulk_download_file_name":"Extracellular_signal_regulated_protein_k.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844842/h8190102175-libre.pdf?1708956265=\u0026response-content-disposition=attachment%3B+filename%3DExtracellular_signal_regulated_protein_k.pdf\u0026Expires=1740039264\u0026Signature=NI4u5X57MGvoRHAGu-1gqCENoc2gwiArmYoavfQAGCUqyXX1Gyrl9IcEATAg4qe~nN62Z2vmQhj4uZ8vXDL06kHXte5vjchy6SEnIEEkqKD6Ur-GtY9qEal53ka1QxWvcdowTBbWfqh1nCuxbbDOP7W2EbyspfD4qCJ5SyWV4yhTdyTLiGvlL7zDBPFJVtElOAu97s8eQIg9tPREJyAi3PHQyEvBXTM~PsKvLj2nJcktQkL6GDGH8a-c9ns2wkq8Z2K5OFdT45Vuk2mgaaz6H6PaJvk6dsuZa4KBu1nHeB9fvvrkMP7-zqixVgbM6u3qlw-N3itDD62aD-xOumCDcw__\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="115437734"><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/115437734/CD105_inhibits_transforming_growth_factor_beta_Smad3_signalling"><img alt="Research paper thumbnail of CD105 inhibits transforming growth factor-beta-Smad3 signalling" 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/115437734/CD105_inhibits_transforming_growth_factor_beta_Smad3_signalling">CD105 inhibits transforming growth factor-beta-Smad3 signalling</a></div><div class="wp-workCard_item"><span>PubMed</span><span>, Jul 28, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">CD105 (endoglin) is an important component of the transforming growth factor-beta (TGF-beta) rece...</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">CD105 (endoglin) is an important component of the transforming growth factor-beta (TGF-beta) receptor complex and is highly expressed in endothelial cells in tissues undergoing angiogenesis such as healing wounds, infarcts and in a wide range of tumours. In an attempt to understand the molecular mechanism by which CD105 exerts its effects on angiogenesis by modulating TGF-beta1 signalling, in this preliminary communication, CD105 transfected rat myoblasts were utilized as an in vitro model. Overexpression of CD105 in these transfectants antagonised TGF-beta1-mediated inhibition of cell proliferation and reduced TGF-beta1-mediated p3TP-Lux (PAI-1 promoter) luciferase activity. It also reduced (CAGA)12-Luc luciferase activity in response to TGF-beta1. The CAGA sequence is specific for Smad3/4 binding, implying that CD105 is involved in inhibition of TGF-beta1/Smad3 signalling. Furthermore, CD105 overexpression reduced serine phosphorylation of Smad3 and inhibited subsequent nuclear translocation of Smad3. CD105 resulted in high phosphorylation of JNK1, which is able to activate c-Jun. c-Jun is known to inhibit Smad3 transcriptional activity on CAGA sites, suggesting that CD105 may also inhibit Smad3 signalling through JNK1.</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="115437734"><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="115437734"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437734; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437734]").text(description); $(".js-view-count[data-work-id=115437734]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437734; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437734']"); 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" } } $('.js-work-strip[data-work-id=115437734]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437734,"title":"CD105 inhibits transforming growth factor-beta-Smad3 signalling","internal_url":"https://www.academia.edu/115437734/CD105_inhibits_transforming_growth_factor_beta_Smad3_signalling","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"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="115437733"><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/115437733/Homozygous_i_GDF2_i_nonsense_mutations_result_in_a_loss_of_circulating_BMP9_and_BMP10_and_are_associated_with_either_PAH_or_an_HHT_like_syndrome_in_children"><img alt="Research paper thumbnail of Homozygous <i>GDF2</i> nonsense mutations result in a loss of circulating BMP9 and BMP10 and are associated with either PAH or an “HHT‐like” syndrome in children" class="work-thumbnail" src="https://attachments.academia-assets.com/111844838/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/115437733/Homozygous_i_GDF2_i_nonsense_mutations_result_in_a_loss_of_circulating_BMP9_and_BMP10_and_are_associated_with_either_PAH_or_an_HHT_like_syndrome_in_children">Homozygous <i>GDF2</i> nonsense mutations result in a loss of circulating BMP9 and BMP10 and are associated with either PAH or an “HHT‐like” syndrome in children</a></div><div class="wp-workCard_item"><span>Molecular Genetics & Genomic Medicine</span><span>, Apr 9, 2021</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">This is an open access article under the terms of the Creative Commons Attribution License, which...</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">This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1268870917713eb78bfc8b853f81a069" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844838,"asset_id":115437733,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844838/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="115437733"><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="115437733"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437733; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "1268870917713eb78bfc8b853f81a069" } } $('.js-work-strip[data-work-id=115437733]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437733,"title":"Homozygous \u003ci\u003eGDF2\u003c/i\u003e nonsense mutations result in a loss of circulating BMP9 and BMP10 and are associated with either PAH or an “HHT‐like” syndrome in children","internal_url":"https://www.academia.edu/115437733/Homozygous_i_GDF2_i_nonsense_mutations_result_in_a_loss_of_circulating_BMP9_and_BMP10_and_are_associated_with_either_PAH_or_an_HHT_like_syndrome_in_children","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"attachments":[{"id":111844838,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844838/thumbnails/1.jpg","file_name":"mggm_Hodgson_2021.pdf","download_url":"https://www.academia.edu/attachments/111844838/download_file","bulk_download_file_name":"Homozygous_i_GDF2_i_nonsense_mutations_r.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844838/mggm_Hodgson_2021-libre.pdf?1708956268=\u0026response-content-disposition=attachment%3B+filename%3DHomozygous_i_GDF2_i_nonsense_mutations_r.pdf\u0026Expires=1740039264\u0026Signature=MU7r5AMlg-7-4Ou0~YVYGZWFvte9NgaIXsLO36TPUbDuQ2GV90RyMDSYKBf0rwnWJhzYgNi5TI5OXvFbOQneLoXVUoN-MKyzUzOhP-hCIPg9TSyItBWCECasDPl1PVio~EzNiTK9Cc8pzn0VreY0Az7k-Nlb4qXeVegAkMHTdYw3WbkC0~vNQQ42F8gnsU01WYtn-KOlgsDDNUzSKBW71480oCCK~V1I2aUfnLLppz4uPzKWrLMmH3nakUfwjoo2u4ONMGTJ2eyzpw~P8s8L~zEOcQlJ1uCMyYOkEVfjzMBta1TuR43QOqvqApcikkADuWgTx4D6EVEE6vpftuNp~g__\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="115437732"><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/115437732/Correlation_Between_Endoglin_and_Malignant_Phenotype_in_Human_Melanoma_Cells_Analysis_of_hsa_mir_214_and_hsa_mir_370_in_Cells_and_Their_Extracellular_Vesicles"><img alt="Research paper thumbnail of Correlation Between Endoglin and Malignant Phenotype in Human Melanoma Cells: Analysis of hsa-mir-214 and hsa-mir-370 in Cells and Their Extracellular Vesicles" class="work-thumbnail" src="https://attachments.academia-assets.com/111844804/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/115437732/Correlation_Between_Endoglin_and_Malignant_Phenotype_in_Human_Melanoma_Cells_Analysis_of_hsa_mir_214_and_hsa_mir_370_in_Cells_and_Their_Extracellular_Vesicles">Correlation Between Endoglin and Malignant Phenotype in Human Melanoma Cells: Analysis of hsa-mir-214 and hsa-mir-370 in Cells and Their Extracellular Vesicles</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Endoglin (CD105) is an auxiliary receptor of transforming growth factor (TGF)-b family members th...</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">Endoglin (CD105) is an auxiliary receptor of transforming growth factor (TGF)-b family members that is expressed in human melanomas. It is heterogeneously expressed by primary and metastatic melanoma cells, and endoglin targeting as a therapeutic strategy for melanoma tumors is currently been explored. However, its involvement in tumor development and malignancy is not fully understood. Here, we find that endoglin expression correlates with malignancy of primary melanomas and cultured melanoma cell lines. Next, we have analyzed the effect of ectopic endoglin expression on two miRNAs (hsa-mir-214 and hsa-mir-370), both involved in melanoma tumor progression and endoglin regulation. We show that compared with control cells, overexpression of endoglin in the WM-164 melanoma cell line induces; (i) a significant increase of hsa-mir-214 levels in small extracellular vesicles (EVs) as well as an increased trend in cells; and (ii) significantly lower levels of hsa-mir-370 in the EVs fractions, whereas no significant differences were found in cells. As hsa-mir-214 and hsa-mir-370 are not just involved in melanoma tumor progression, but they can also target endoglin-expressing endothelial cells in the tumor vasculature, these results suggest a complex and differential regulatory mechanism involving the intracellular and extracellular signaling of</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="8232fb8408a3b008e5089c3c2c3f7cad" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844804,"asset_id":115437732,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844804/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="115437732"><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="115437732"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437732; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437732]").text(description); $(".js-view-count[data-work-id=115437732]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437732; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437732']"); 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: "8232fb8408a3b008e5089c3c2c3f7cad" } } $('.js-work-strip[data-work-id=115437732]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437732,"title":"Correlation Between Endoglin and Malignant Phenotype in Human Melanoma Cells: Analysis of hsa-mir-214 and hsa-mir-370 in Cells and Their Extracellular Vesicles","internal_url":"https://www.academia.edu/115437732/Correlation_Between_Endoglin_and_Malignant_Phenotype_in_Human_Melanoma_Cells_Analysis_of_hsa_mir_214_and_hsa_mir_370_in_Cells_and_Their_Extracellular_Vesicles","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"attachments":[{"id":111844804,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844804/thumbnails/1.jpg","file_name":"978-3-031-26163-3_14.pdf","download_url":"https://www.academia.edu/attachments/111844804/download_file","bulk_download_file_name":"Correlation_Between_Endoglin_and_Maligna.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844804/978-3-031-26163-3_14-libre.pdf?1708956273=\u0026response-content-disposition=attachment%3B+filename%3DCorrelation_Between_Endoglin_and_Maligna.pdf\u0026Expires=1740039264\u0026Signature=dFJ~XjO0ofqsHLIsQF5XT3UF1CvBFZ5F7qEavJzWmqjQT-YdV~k-SpFCgvoqbE7UIBQ-PhIUJNjW6z0ydClD87C8RXCdQx-4Bz4bxbsgtqliCTu28vucuT3XcqFaHENF7C53mCVN87tmr1H2Vu3TOICSGNeURVqsLU1r~Z3qRzp4Thw1UxUXZLP8BeZwiEfVpyj-oQbIeDtOPYoBOv9gu6otXo7CiinhMIdX44TNC1SaBEdyTo0sXdv6ULANeG~Cy7KP8AUmsRxSxEvbFa9136kzkRYgTC0Rnle-pkpEfusgEPet6sJFPS3K8x9TcGKWqbwrDtuPH4N6v2ng-KeCng__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":111844805,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844805/thumbnails/1.jpg","file_name":"978-3-031-26163-3_14.pdf","download_url":"https://www.academia.edu/attachments/111844805/download_file","bulk_download_file_name":"Correlation_Between_Endoglin_and_Maligna.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844805/978-3-031-26163-3_14-libre.pdf?1708956267=\u0026response-content-disposition=attachment%3B+filename%3DCorrelation_Between_Endoglin_and_Maligna.pdf\u0026Expires=1740039264\u0026Signature=W-9wDSGCYXAWAOT2eYEjW2jw~McahABtF7WH6xSYuQOIKitkdrmOXEJVvRzE8cSO3MHPfVP90OJLnU7xY2~TuVkZ7xcSTIDMIvMY9paQ~JGIKQPnrs-9Nx5EYAbnXWc-sE3bYLgPkTwlvLj8Sib-rag602ntS1BE9DkyFxwNJj9JzefoShr~-yxvPZRcOSGNLmuJgn7E0vF-ageaSWuRkAfjzwd4C8oON6ApTUJNJf0RQDelze84K8lfcfA7Ut4-kwBpXI5kROmlPgbMFyLrLFcWVy3FQ985x3vxKIo3gRLsOShXDAVv72-a9BSPh4geu3hbzEweWQh8rNuuHlQewg__\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="115437730"><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/115437730/TGF_%CE%B2_Signalling_and_Its_Role_in_Cancer_Progression_and_Metastasis"><img alt="Research paper thumbnail of TGF-β Signalling and Its Role in Cancer Progression and Metastasis" class="work-thumbnail" src="https://attachments.academia-assets.com/111844840/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/115437730/TGF_%CE%B2_Signalling_and_Its_Role_in_Cancer_Progression_and_Metastasis">TGF-β Signalling and Its Role in Cancer Progression and Metastasis</a></div><div class="wp-workCard_item"><span>eLS</span><span>, Aug 16, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The transforming growth factor-β (TGF-β) system signals via protein kinase receptors and SMAD med...</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 transforming growth factor-β (TGF-β) system signals via protein kinase receptors and SMAD mediators to regulate a large number of biological processes. Alterations of the TGF-β signalling pathway are implicated in human cancer. Prior to tumour initiation and early during progression, TGF-β acts as a tumour suppressor; however, at later stages, it is often a tumour promoter. Knowledge about the mechanisms involved in TGF-β signal transduction has allowed a better understanding of cancer progression, invasion, metastasis and epithelial-to-mesenchymal transition. Furthermore, several molecular targets with great potential in therapeutic interventions have been identified. This review discusses the TGF-β signalling pathway, its involvement in cancer and current therapeutic approaches.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="287a2ab438714898c496aac9aaff735f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844840,"asset_id":115437730,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844840/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="115437730"><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="115437730"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437730; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437730]").text(description); $(".js-view-count[data-work-id=115437730]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437730; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437730']"); 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: "287a2ab438714898c496aac9aaff735f" } } $('.js-work-strip[data-work-id=115437730]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437730,"title":"TGF-β Signalling and Its Role in Cancer Progression and Metastasis","internal_url":"https://www.academia.edu/115437730/TGF_%CE%B2_Signalling_and_Its_Role_in_Cancer_Progression_and_Metastasis","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"attachments":[{"id":111844840,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844840/thumbnails/1.jpg","file_name":"s10555-012-9375-720240226-1-eaq274.pdf","download_url":"https://www.academia.edu/attachments/111844840/download_file","bulk_download_file_name":"TGF__Signalling_and_Its_Role_in_Cancer.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844840/s10555-012-9375-720240226-1-eaq274-libre.pdf?1708956268=\u0026response-content-disposition=attachment%3B+filename%3DTGF__Signalling_and_Its_Role_in_Cancer.pdf\u0026Expires=1740039264\u0026Signature=Ru3Vc3-rm6D1~--CVOW20SIs1pydyOLng-1V-Ywwd9g9KsCQArwYc59M6CMZ~YgWM01HvQ5~g-JUn1jwSXkE~-erfbcRXRtduLLMfdnRJVeClNCeH1ztCbulwadPV~1oW19KP3JULK~mQ6SKPN9QXIf9Meq-o7wwI-NU25rtDwSWLVsctR~HPXy6LsxaWI0b-H5cn3Sfqo3UFrDsLExHpHX8jYCm0ktFE7fpAlW-05b4ZFr-txwIbDMRM5PvYQupF~sioFXthcCO-9n9st~yN1W8dJgC~EVhAD97WHyI2U4SvH5nEixtx0YE-MqwLNp4r8ROTssaG1B6G3YmoViNgA__\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="115437729"><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/115437729/Expression_of_the_major_histocompatibility_antigens_HLA_A2_and_HLA_B7_by_DNA_mediated_gene_transfer"><img alt="Research paper thumbnail of Expression of the major histocompatibility antigens HLA-A2 and HLA-B7 by DNA-mediated gene transfer" class="work-thumbnail" src="https://attachments.academia-assets.com/111844841/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/115437729/Expression_of_the_major_histocompatibility_antigens_HLA_A2_and_HLA_B7_by_DNA_mediated_gene_transfer">Expression of the major histocompatibility antigens HLA-A2 and HLA-B7 by DNA-mediated gene transfer</a></div><div class="wp-workCard_item"><span>Journal of Immunology</span><span>, Oct 1, 1983</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">T-lymphocytic infiltration of the exocrine pancreas and liver in patients with chronic pancreatit...</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">T-lymphocytic infiltration of the exocrine pancreas and liver in patients with chronic pancreatitis has suggested that cell mediated immune mechanisms may play a part in the pathogenesis of this disease. As expression of major histocompatibility (MHC) antigens is a prerequisite for organ specific autoimmunity, the expression of HLA class I (P2-micro</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0004b386c3233f9b9193b966214b7430" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844841,"asset_id":115437729,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844841/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="115437729"><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="115437729"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437729; 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They a r e a l t e r e d i n tufA and tufis, the two genes coding f o r the elongation f a c t o r EF-Tu. One of these genes can be i n a c t i v a t e d by i n s e r t i o n of bacteriophage Mu. This enabled us t o study t h e nature and funct i o n o f t h e mutant EF-Tu s p e c i e s (c. f. a l s o F. J .</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c85904676a7284346d155952c1b033cf" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844837,"asset_id":115437727,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844837/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="115437727"><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="115437727"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437727; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="115437723"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/115437723/Editorial_Role_of_membrane_bound_and_circulating_endoglin_in_disease"><img alt="Research paper thumbnail of Editorial: Role of membrane-bound and circulating endoglin in disease" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/115437723/Editorial_Role_of_membrane_bound_and_circulating_endoglin_in_disease">Editorial: Role of membrane-bound and circulating endoglin in disease</a></div><div class="wp-workCard_item"><span>Frontiers in Medicine</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="115437723"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="115437723"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437723; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=115437723]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437723,"title":"Editorial: Role of membrane-bound and circulating endoglin in disease","internal_url":"https://www.academia.edu/115437723/Editorial_Role_of_membrane_bound_and_circulating_endoglin_in_disease","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"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="115437722"><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/115437722/Monoclonal_anti_endoglin_antibody_TRC105_carotuximab_prevents_hypercholesterolemia_and_hyperglycemia_induced_endothelial_dysfunction_in_human_aortic_endothelial_cells"><img alt="Research paper thumbnail of Monoclonal anti-endoglin antibody TRC105 (carotuximab) prevents hypercholesterolemia and hyperglycemia-induced endothelial dysfunction in human aortic endothelial cells" class="work-thumbnail" src="https://attachments.academia-assets.com/111844843/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/115437722/Monoclonal_anti_endoglin_antibody_TRC105_carotuximab_prevents_hypercholesterolemia_and_hyperglycemia_induced_endothelial_dysfunction_in_human_aortic_endothelial_cells">Monoclonal anti-endoglin antibody TRC105 (carotuximab) prevents hypercholesterolemia and hyperglycemia-induced endothelial dysfunction in human aortic endothelial cells</a></div><div class="wp-workCard_item"><span>Frontiers in Medicine</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Endoglin (Eng) is a co-receptor of the transforming growth factor β superfamily playing an import...</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">Endoglin (Eng) is a co-receptor of the transforming growth factor β superfamily playing an important role in endothelial dysfunction. TRC105 (carotuximab) is a monoclonal antibody that blocks Eng and its downstream Smad signaling pathway. Here we have investigated for the first time the effects of TRC105 treatment on the development of endothelial dysfunction induced by 7-ketocholesterol (7K) or high glucose (HG), focusing on Eng expression, signaling, and function. In the hypercholesterolemia study, human aortic endothelial cells (HAoECs) were treated with TRC105 (300 μg/ml) for 1 h, followed by the addition of 7K (10 μg/ml) for another 12 h. In the hyperglycemia study, HAoECs were exposed to HG (45 mM) for 60 h, followed by the addition of TRC105 for another 12 h, and cells treated with 5mM glucose and 40 mM mannitol served as control. Protein levels, adhesion, and transmigration of monocytes were assessed by flow cytometry, mRNA expression was measured by qRT-PCR. 7K and HG treat...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="cb69a7ad6276d29671d7926e61e36d30" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844843,"asset_id":115437722,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844843/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="115437722"><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="115437722"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437722; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437722]").text(description); $(".js-view-count[data-work-id=115437722]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437722; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437722']"); 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: "cb69a7ad6276d29671d7926e61e36d30" } } $('.js-work-strip[data-work-id=115437722]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437722,"title":"Monoclonal anti-endoglin antibody TRC105 (carotuximab) prevents hypercholesterolemia and hyperglycemia-induced endothelial dysfunction in human aortic endothelial cells","internal_url":"https://www.academia.edu/115437722/Monoclonal_anti_endoglin_antibody_TRC105_carotuximab_prevents_hypercholesterolemia_and_hyperglycemia_induced_endothelial_dysfunction_in_human_aortic_endothelial_cells","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"attachments":[{"id":111844843,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844843/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/111844843/download_file","bulk_download_file_name":"Monoclonal_anti_endoglin_antibody_TRC105.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844843/pdf-libre.pdf?1708956273=\u0026response-content-disposition=attachment%3B+filename%3DMonoclonal_anti_endoglin_antibody_TRC105.pdf\u0026Expires=1740039264\u0026Signature=IwkiBl5596jlRx~XYP59HvHUAVjpZhYppbxRfjngKIR1fuDqRTzM~mkhtv4raPl~Su9uTdidhOgXvIw0LrNwfoMyNVOhNUETkFod4WjzIuCsr3bEHMBSYLWlvXOWc2DrMeFISsa9kYvv8015vlhjtFntgb-lL~yO3UAwdu7ie-RQVsA1Ud8EhtoWe-DLaRmR4To43QfYxvLzEW634YfDr~TlwrZCOsUUVZmvUUKE7974QvEk2ebQyuZ~Di~thRposbmPCoOImcx~J8E9DoLXRh14Kp1PZwU-xh~xnRIFAStxUWLQWNNKuAP8MmO6-mMQLinC6alAZ5dNt8yZqxerBQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="115437721"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/115437721/Novel_vascular_roles_of_human_endoglin_in_pathophysiology"><img alt="Research paper thumbnail of Novel vascular roles of human endoglin in pathophysiology" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/115437721/Novel_vascular_roles_of_human_endoglin_in_pathophysiology">Novel vascular roles of human endoglin in pathophysiology</a></div><div class="wp-workCard_item"><span>Journal of Thrombosis and Haemostasis</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="115437721"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="115437721"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437721; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437721]").text(description); $(".js-view-count[data-work-id=115437721]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437721; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437721']"); 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" } } $('.js-work-strip[data-work-id=115437721]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437721,"title":"Novel vascular roles of human endoglin in pathophysiology","internal_url":"https://www.academia.edu/115437721/Novel_vascular_roles_of_human_endoglin_in_pathophysiology","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"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="115437719"><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/115437719/Emerging_role_of_endothelial_endoglin_in_integrin_mediated_cell_adhesion"><img alt="Research paper thumbnail of Emerging role of endothelial endoglin in integrin-mediated cell adhesion" class="work-thumbnail" src="https://attachments.academia-assets.com/111844836/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/115437719/Emerging_role_of_endothelial_endoglin_in_integrin_mediated_cell_adhesion">Emerging role of endothelial endoglin in integrin-mediated cell adhesion</a></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="4dbf24569f5214ae6c808f04ab203304" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844836,"asset_id":115437719,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844836/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="115437719"><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="115437719"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437719; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=115437719]").text(description); $(".js-view-count[data-work-id=115437719]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 115437719; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='115437719']"); 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: "4dbf24569f5214ae6c808f04ab203304" } } $('.js-work-strip[data-work-id=115437719]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":115437719,"title":"Emerging role of endothelial endoglin in integrin-mediated cell adhesion","internal_url":"https://www.academia.edu/115437719/Emerging_role_of_endothelial_endoglin_in_integrin_mediated_cell_adhesion","owner_id":33247403,"coauthors_can_edit":true,"owner":{"id":33247403,"first_name":"Carmelo","middle_initials":null,"last_name":"Bernabeu","page_name":"CarmeloBernabeu","domain_name":"csic","created_at":"2015-07-22T02:03:56.418-07:00","display_name":"Carmelo Bernabeu","url":"https://csic.academia.edu/CarmeloBernabeu"},"attachments":[{"id":111844836,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/111844836/thumbnails/1.jpg","file_name":"jmm2017.pdf","download_url":"https://www.academia.edu/attachments/111844836/download_file","bulk_download_file_name":"Emerging_role_of_endothelial_endoglin_in.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/111844836/jmm2017-libre.pdf?1708956260=\u0026response-content-disposition=attachment%3B+filename%3DEmerging_role_of_endothelial_endoglin_in.pdf\u0026Expires=1740039264\u0026Signature=B~ydaUSfuv7IyAm5O4vfGJKZ9cBwB~Cy6pVCSoIZo3RPz2p-zj1fsNSCLCCZxMd4Hj6xJJteYRANq9xZjD9BsffYtWXpVCgczUWC6qsPrKWXEOHOFuxiZjUvS3aeGIzjOZGmX3-qXbWpwXw-eJuZcGxhBS~2PAm6InIrA~R84lbURdSkyFdA~gvwX0XeFyqMhe4O6IMRSqAPkefJ8yWVaxAV0LEl5wgsYVTukqHwHVKUI~V32aU1Es2UYkrhoObm4rGL~J~B05QhSrNj6l4rzmahUZZvSF-swHRVKjUiMa8W5qJ0TtZYty-1aHPORiujCE8R6-iqSx0hGT2-59nIpQ__\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="115437718"><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/115437718/The_Tgf_%CE%B2_Bmp_Co_Receptor_Endoglin_Is_a_Key_Component_of_the_Molecular_Oscillator_That_Regulates_the_Hair_Follicle_Cycle"><img alt="Research paper thumbnail of The Tgf-β/Bmp Co-Receptor Endoglin Is a Key Component of the Molecular Oscillator That Regulates the Hair Follicle Cycle" class="work-thumbnail" src="https://attachments.academia-assets.com/111844991/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/115437718/The_Tgf_%CE%B2_Bmp_Co_Receptor_Endoglin_Is_a_Key_Component_of_the_Molecular_Oscillator_That_Regulates_the_Hair_Follicle_Cycle">The Tgf-β/Bmp Co-Receptor Endoglin Is a Key Component of the Molecular Oscillator That Regulates the Hair Follicle Cycle</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The hair follicle is a biological oscillator that alternates growth, regression, and rest phases ...</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 hair follicle is a biological oscillator that alternates growth, regression, and rest phases driven by the sequential activation of the proliferation/differentiation programs of resident stem cell populations. The activation of hair follicle stem cell niches and subsequent entry into the growing phase is mainly regulated by Wnt/β-catenin signalling, while regression and resting phases are mainly regulated by Tgf-β/Bmp/Smad activity. A major question still unresolved is the nature of the molecular switch that dictates the coordinated transition between both signalling pathways. Here we have focused on the role of Endoglin (Eng), a key co-receptor for members of the Tgfβ/Bmp family of growth factors. Using an Eng haploinsufficient mouse model, we report that Eng is required to maintain a correct follicle cycling pattern and for an adequate stimulation of hair follicle stem cell niches. We further report that β-catenin binds to the Eng promoter depending on Bmp signalling. Moreover, we show that β-catenin interacts with Smad4 in a Bmp/Eng-dependent context and both proteins act synergistically to activate Eng promoter transcription. These observations point to the existence of a growth/rest switching mechanism in the hair follicle that is based on an Eng-dependent feedback cross-talk between Wnt/β-catenin and Bmp/Smad signals.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="769b17ac2ba07345f196e82cf25c083f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":111844991,"asset_id":115437718,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/111844991/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="115437718"><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="115437718"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437718; 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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="115437717"><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/115437717/Mapping_the_Ribosomal_Exit_Site_of_the_Nascent_Polypeptide_Chain_by_Immune_Electron_Microscopy"><img alt="Research paper thumbnail of Mapping the Ribosomal Exit Site of the Nascent Polypeptide Chain by Immune Electron Microscopy" 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/115437717/Mapping_the_Ribosomal_Exit_Site_of_the_Nascent_Polypeptide_Chain_by_Immune_Electron_Microscopy">Mapping the Ribosomal Exit Site of the Nascent Polypeptide Chain by Immune Electron Microscopy</a></div><div class="wp-workCard_item"><span>Proceedings, annual meeting, Electron Microscopy Society of America</span><span>, 1981</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Immune electron microscopy is providing information on the three dimensional locations of many fu...</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">Immune electron microscopy is providing information on the three dimensional locations of many functional sites on the ribosome. In particular, localization of the exit site of the newly synthesized protein chain is expected to provide information on the mechanisms of protein synthesis and on the nature of the ribosome-membrane association. Theoretically the nascent chains of the largest proteins could be visible as they leave the ribosome, but in practice they have not been observed. In order to map their exit site we have made antibodies against one particular enzyme and then applied immune electron microscopy to a polysome fraction enriched for that special protein.In a mutant of Escherichia coli constitutive for the enzyme beta-galac- tosidase, this enzyme accounts for approximately 25% of the total protein (1). Because of the high molecular weight of beta-galactosidase, a fraction of larger polysomes, further enriched in this emzyme, was obtained by differential centrifugation....</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="115437717"><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="115437717"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 115437717; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); 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