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

Publication ,  Journal Article
Paulsson, AK; Franklin, S; Mitchell-Jordan, SA; Ren, S; Wang, Y; Vondriska, TM
Published in: J Mol Cell Cardiol
June 2010

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.

Duke Scholars

Published In

J Mol Cell Cardiol

DOI

EISSN

1095-8584

Publication Date

June 2010

Volume

48

Issue

6

Start / End Page

1206 / 1214

Location

England

Related Subject Headings

  • Sequence Homology, Amino Acid
  • Proteomics
  • Protein Processing, Post-Translational
  • Phosphorylation
  • Myocardium
  • Muscle Proteins
  • Molecular Sequence Data
  • Microfilament Proteins
  • Mice, Inbred BALB C
  • Mice
 

Citation

APA
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ICMJE
MLA
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Paulsson, A. K., Franklin, S., Mitchell-Jordan, S. A., Ren, S., Wang, Y., & Vondriska, T. M. (2010). Post-translational regulation of calsarcin-1 during pressure overload-induced cardiac hypertrophy. J Mol Cell Cardiol, 48(6), 1206–1214. https://doi.org/10.1016/j.yjmcc.2010.02.009
Paulsson, Anna K., Sarah Franklin, Scherise A. Mitchell-Jordan, Shuxun Ren, Yibin Wang, and Thomas M. Vondriska. “Post-translational regulation of calsarcin-1 during pressure overload-induced cardiac hypertrophy.J Mol Cell Cardiol 48, no. 6 (June 2010): 1206–14. https://doi.org/10.1016/j.yjmcc.2010.02.009.
Paulsson AK, Franklin S, Mitchell-Jordan SA, Ren S, Wang Y, Vondriska TM. Post-translational regulation of calsarcin-1 during pressure overload-induced cardiac hypertrophy. J Mol Cell Cardiol. 2010 Jun;48(6):1206–14.
Paulsson, Anna K., et al. “Post-translational regulation of calsarcin-1 during pressure overload-induced cardiac hypertrophy.J Mol Cell Cardiol, vol. 48, no. 6, June 2010, pp. 1206–14. Pubmed, doi:10.1016/j.yjmcc.2010.02.009.
Paulsson AK, Franklin S, Mitchell-Jordan SA, Ren S, Wang Y, Vondriska TM. Post-translational regulation of calsarcin-1 during pressure overload-induced cardiac hypertrophy. J Mol Cell Cardiol. 2010 Jun;48(6):1206–1214.
Journal cover image

Published In

J Mol Cell Cardiol

DOI

EISSN

1095-8584

Publication Date

June 2010

Volume

48

Issue

6

Start / End Page

1206 / 1214

Location

England

Related Subject Headings

  • Sequence Homology, Amino Acid
  • Proteomics
  • Protein Processing, Post-Translational
  • Phosphorylation
  • Myocardium
  • Muscle Proteins
  • Molecular Sequence Data
  • Microfilament Proteins
  • Mice, Inbred BALB C
  • Mice