Post-translational regulation of calsarcin-1 during pressure overload-induced cardiac hypertrophy.

ABSTRACT: Chronic pressure overload to the heart leads to cardiac hypertrophy and failure through processes that involve reorganization of subcellular compartments and alteration of established signaling mechanisms. To identify proteins contributing to this process, we examined changes in nuclear-associated myofilament proteins as the murine heart undergoes progressive hypertrophy following pressure overload. Calsarcin-1, a negative regulator of calcineurin signaling in the heart, was found to be enriched in cardiac nuclei and displays increased abundance following pressure overload through a mechanism that is decoupled from transcriptional regulation. Using proteomics, we identified novel processing of this protein in the setting of cardiac injury and identified four residues subject to modificatio

SUBMITTER: Paulsson AK 

PROVIDER: S-EPMC2866759 | biostudies-literature | 2010 Jun

REPOSITORIES: biostudies-literature