<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lerchenmuller C</submitter><funding>NCATS NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>1854-67</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5001879</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>36(9)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>S100A6, a member of the S100 protein family, has been described as relevant for cell cycle entry and progression in endothelial cells. The molecular mechanism conferring S100A6's proliferative actions, however, remained elusive.&lt;h4>Approach and results&lt;/h4>Originating from the clinically relevant observation of enhanced S100A6 protein expression in proliferating endothelial cells in remodeling coronary and carotid arteries, our study unveiled S100A6 as a suppressor of antiproliferative signal transducers and activators of transcription 1 signaling. Discovery of the molecular liaison was enabled by combining gene expression time series analysis with bioinformatic pathway modeling in S100A6-silenced human endothelial cells stimulated with vascular endothelial growth factor </pubmed_abstract><journal>Arteriosclerosis, thrombosis, and vascular biology</journal><pubmed_title>S100A6 Regulates Endothelial Cell Cycle Progression by Attenuating Antiproliferative Signal Transducers and Activators of Transcription 1 Signaling.</pubmed_title><pmcid>PMC5001879</pmcid><funding_grant_id>UL1 TR001102</funding_grant_id><funding_grant_id>T32 HL007374</funding_grant_id><pubmed_authors>Lerchenmuller C</pubmed_authors><pubmed_authors>Damilano F</pubmed_authors><pubmed_authors>Most P</pubmed_authors><pubmed_authors>Bochaton-Piallat ML</pubmed_authors><pubmed_authors>Busch H</pubmed_authors><pubmed_authors>Peppel K</pubmed_authors><pubmed_authors>Heißenberg J</pubmed_authors><pubmed_authors>Bezzeridis VJ</pubmed_authors><pubmed_authors>Rosenzweig A</pubmed_authors><pubmed_authors>Katus HA</pubmed_authors><pubmed_authors>Boerries M</pubmed_authors><pubmed_authors>Busch M</pubmed_authors><pubmed_authors>Hirschberg K</pubmed_authors><pubmed_authors>Kramer I</pubmed_authors></additional><is_claimable>false</is_claimable><name>S100A6 Regulates Endothelial Cell Cycle Progression by Attenuating Antiproliferative Signal Transducers and Activators of Transcription 1 Signaling.</name><description>&lt;h4>Objective&lt;/h4>S100A6, a member of the S100 protein family, has been described as relevant for cell cycle entry and progression in endothelial cells. The molecular mechanism conferring S100A6's proliferative actions, however, remained elusive.&lt;h4>Approach and results&lt;/h4>Originating from the clinically relevant observation of enhanced S100A6 protein expression in proliferating endothelial cells in remodeling coronary and carotid arteries, our study unveiled S100A6 as a suppressor of antiproliferative signal transducers and activators of transcription 1 signaling. Discovery of the molecular liaison was enabled by combining gene expression time series analysis with bioinformatic pathway modeling in S100A6-silenced human endothelial cells stimulated with vascular endothelial growth factor </description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Sep</publication><modification>2026-04-29T01:12:11.525Z</modification><creation>2019-03-27T02:22:49Z</creation></dates><accession>S-EPMC5001879</accession><cross_references><pubmed>27386938</pubmed><doi>10.1161/ATVBAHA.115.306415</doi><doi>10.1161/atvbaha.115.306415</doi></cross_references></HashMap>