Post-translational regulation of calsarcin-1 during pressure overload-induced cardiac hypertrophy.
J Mol Cell Cardiol
; 48(6): 1206-14, 2010 Jun.
Article
in En
| MEDLINE
| ID: mdl-20170660
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 modification by phosphorylation. These studies are the first to determine mechanisms regulating calsarcin abundance during hypertrophy and failure and reveal the first evidence of post-translational modifications of calsarcin-1 in the myocardium. Overall, the findings expand the roles of calsarcins to include nuclear tasks during cardiac growth.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Carrier Proteins
/
Protein Processing, Post-Translational
/
Gene Expression Regulation
/
Cardiomegaly
/
Muscle Proteins
Type of study:
Prognostic_studies
Limits:
Animals
Language:
En
Journal:
J Mol Cell Cardiol
Year:
2010
Document type:
Article
Affiliation country:
United States