KChIP2 is a core transcriptional regulator of cardiac excitability.

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_Na) and repolarizing (I_to) currents altered in cardiac disease. Genet

SUBMITTER: Nassal DM 

PROVIDER: S-EPMC5338919 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature