La carenza di BRISC determina l'insufficienza cardiaca regolando l'ubiquitina K63 di β-catenina.

BACKGROUND: Adverse cardiac remodeling and dysfunction are hallmarks of hypertensive heart failure, yet molecular mechanisms remain incompletely understood. K63-linked deubiquitination has emerged as a critical posttranslational regulatory process in cardiac remodeling. This study investigated the role of BRISC (BRCC3 [BRCA1/BRCA2-containing complex subunit 3] isopeptidase complex), a K63-specific deubiquitinase, in hypertensive cardiac remodeling. METHODS: Expression of BRISC subunits was analyzed in hypertrophic human and murine hearts. Cardiac phenotypes were assessed in global and cardiomyocyte-specific Abro1 (Abraxas 2, BRISC complex subunit) knockout, cardiomyocyte-specific Abro1 over