{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lerchenmuller C"],"funding":["NCATS NIH HHS","NHLBI NIH HHS"],"pagination":["1854-67"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5001879"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["36(9)"],"pubmed_abstract":["<h4>Objective</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.<h4>Approach and results</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 "],"journal":["Arteriosclerosis, thrombosis, and vascular biology"],"pubmed_title":["S100A6 Regulates Endothelial Cell Cycle Progression by Attenuating Antiproliferative Signal Transducers and Activators of Transcription 1 Signaling."],"pmcid":["PMC5001879"],"funding_grant_id":["UL1 TR001102","T32 HL007374"],"pubmed_authors":["Lerchenmuller C","Damilano F","Most P","Bochaton-Piallat ML","Busch H","Peppel K","Heißenberg J","Bezzeridis VJ","Rosenzweig A","Katus HA","Boerries M","Busch M","Hirschberg K","Kramer I"],"additional_accession":[]},"is_claimable":false,"name":"S100A6 Regulates Endothelial Cell Cycle Progression by Attenuating Antiproliferative Signal Transducers and Activators of Transcription 1 Signaling.","description":"<h4>Objective</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.<h4>Approach and results</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 ","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Sep","modification":"2026-04-29T01:12:11.525Z","creation":"2019-03-27T02:22:49Z"},"accession":"S-EPMC5001879","cross_references":{"pubmed":["27386938"],"doi":["10.1161/ATVBAHA.115.306415","10.1161/atvbaha.115.306415"]}}