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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 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.

journal_name

J Mol Cell Cardiol

journal_title

Journal of molecular and cellular cardiology

authors

Paulsson AK,Franklin S,Mitchell-Jordan SA,Ren S,Wang Y,Vondriska TM

doi

10.1016/j.yjmcc.2010.02.009

subject

Has Abstract

pub_date

2010-06-01 00:00:00

pages

1206-14

issue

6

eissn

0022-2828

issn

1095-8584

pii

S0022-2828(10)00044-1

journal_volume

48

pub_type

杂志文章

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