{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nassal DM"],"funding":["American Heart Association","NHLBI NIH HHS","National Institutes of Health"],"pagination":["e17304"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5338919"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["6"],"pubmed_abstract":["Arrhythmogenesis from aberrant electrical remodeling is a primary cause of death among patients with heart disease. Amongst a multitude of remodeling events, reduced expression of the ion channel subunit KChIP2 is consistently observed in numerous cardiac pathologies. However, it remains unknown if KChIP2 loss is merely a symptom or involved in disease development. Using rat and human derived cardiomyocytes, we identify a previously unobserved transcriptional capacity for cardiac KChIP2 critical in maintaining electrical stability. Through interaction with genetic elements, KChIP2 transcriptionally repressed the miRNAs miR-34b and miR-34c, which subsequently targeted key depolarizing (<i>I</i><sub>Na</sub>) and repolarizing (<i>I</i><sub>to</sub>) currents altered in cardiac disease. Genet"],"journal":["eLife"],"pubmed_title":["KChIP2 is a core transcriptional regulator of cardiac excitability."],"pmcid":["PMC5338919"],"funding_grant_id":["R01 HL096962","R01 HL132520","HL105338-01","13PRE17060106","R01HL132520","R01HL096962"],"pubmed_authors":["Liu H","Maleski D","Moravec CS","Laurita KR","Nassal DM","Ramirez-Navarro A","Wan X","Deschenes I","Ficker E"],"additional_accession":[]},"is_claimable":false,"name":"KChIP2 is a core transcriptional regulator of cardiac excitability.","description":"Arrhythmogenesis from aberrant electrical remodeling is a primary cause of death among patients with heart disease. Amongst a multitude of remodeling events, reduced expression of the ion channel subunit KChIP2 is consistently observed in numerous cardiac pathologies. However, it remains unknown if KChIP2 loss is merely a symptom or involved in disease development. Using rat and human derived cardiomyocytes, we identify a previously unobserved transcriptional capacity for cardiac KChIP2 critical in maintaining electrical stability. Through interaction with genetic elements, KChIP2 transcriptionally repressed the miRNAs miR-34b and miR-34c, which subsequently targeted key depolarizing (<i>I</i><sub>Na</sub>) and repolarizing (<i>I</i><sub>to</sub>) currents altered in cardiac disease. Genet","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Mar","modification":"2026-04-08T17:16:52.62Z","creation":"2019-03-27T02:37:56Z"},"accession":"S-EPMC5338919","cross_references":{"pubmed":["28263709"],"doi":["10.7554/eLife.17304"]}}