Ring finger protein 207 (RNF207)

Ring finger protein 207 (RNF207) is a heart-specific member of the RING finger protein family, predominantly expressed in cardiac tissue[1][4][5]. It contains a zinc-binding RING domain and shares structural features with tripartite motif-containing (TRIM) proteins. RNF207 modulates cardiomyocyte energy metabolism: its depletion leads to mitochondrial dysfunction and reduced ATP levels in cardiac cells[1][4]. RNF207 expression is significantly decreased in models of heart failure. Functionally, RNF207 regulates cardiac electrophysiology by interacting with the HERG (human ether-à-go-go related gene/KCNH2) potassium channel as well as major protein chaperones (HSP70, HSP40/DJA1, HSC70), affecting HERG stability, trafficking, and surface localization[2][5][6][7][8]. This regulation is integral for maintaining proper cardiac action potential and QT interval duration. SNPs in the RNF207 gene have been associated with QT interval prolongation, contributing to arrhythmia risk and Long QT syndrome[2][6][7][8]. RNF207 co-localizes with HERG and modulates quality control of both wild-type and mutant HERG channels. The molecular mechanism involves complex chaperone interactions and may indirectly affect ER export and protein degradation, though RNF207 itself lacks intrinsic E3 ligase activity[2]. RNF207 is under active investigation as a cardiac-specific regulator of excitation and metabolism, especially in the context of inherited or acquired cardiac arrhythmia syndromes and heart failure[1][2][4][6][8]. No direct drug modulators or clinically relevant small molecules targeting RNF207 are currently reported in the literature. If you need disease-specific implications or current research perspectives on RNF207-targeted therapeutics, additional literature review or database search is recommended.

Other names

C1orf188FLJ46380FLJ32096OTTHUMG00000001089RING finger protein 207