Post-translational regulation of calsarcin-1 during pressure overload-induced cardiac hypertrophy
Open accessAbstract
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.
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Thr107 or Thr111 are phosphorylated residues that have been previously confirmed at the peptide level.
“ECD fragmentation of the monophosphorylated and presence of phosphorylated z·-ions suggests that a phosphorylation site may be located at Thr107 or Thr111, phosphorylated residues that have been previously confirmed at the peptide level (39, 40).”
From Distinct hypertrophic cardiomyopathy genotypes result in convergent sarcomeric proteoform profiles revealed by top-down proteomics (2020) · cites this paper as [39]
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Tucholski, T., Cai, W., Gregorich, Z. R., Bayne, E. F., Mitchell, S. D., McIlwain, S. J., de Lange, W. J., Wrobbel, M., Karp, H., Hite, Z., et al. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2006764117 · Cited by 107 · see citing works
- Authors
- Paulsson, A. K., Franklin, S., Mitchell-Jordan, S. A., Ren, S., Wang, Y., & Vondriska, T. M.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Vondriska, Thomas M.
- Venue
- Journal of Molecular and Cellular Cardiology
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 48
- Issue
- 6
- Pages
- 1206-1214
- ISSN
- 0022-2828 (ISSN-L)
- PMC
- PMC2866759
- OpenAlex
- W2030243614
- Cited by
- 16
- References
- 20
- Citations by year
- 2020: 1 · 2018: 2 · 2017: 1 · 2015: 2 · 2014: 2 · 2012: 3
- FWCI
- 1.04
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Molecular and Cellular Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Keywords
- cardiac hypertrophy, pressure overload, post-translational modification, phosphorylation, calcineurin signaling, heart failure, myocardium, protein processing
- MeSH terms
- Amino Acid Sequence, Animals, Carrier Proteins, Gene Expression Regulation, Cardiomegaly, Hypertrophy, Male, Mice, Inbred BALB C, Microfilament Proteins, Molecular Sequence Data, Muscle Proteins, Myocardium, Phosphorylation, Protein Processing, Post-Translational, Sequence Homology, Amino Acid, Proteomics, Mice
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