ArticleThe Journal of biological chemistry2010
Phosphorylation of cardiac troponin I at protein kinase C site threonine 144 depresses cooperative activation of thin filaments.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Evidence for a role of adverse sarcomere signaling in atrial fibrillation induction.Journal of molecular and cellular cardiology plus · 2026Review
- Troponin I - a comprehensive review of its function, structure, evolution, and role in muscle diseases.Animal cells and systems · 2025Review
- Fluorescence lifetime-based assay reports structural changes in cardiac muscle mediated by effectors of contractile regulation.The Journal of general physiology · 2023Article
- A Selective Inhibitor of Cardiac Troponin I Phosphorylation by Delta Protein Kinase C (δPKC) as a Treatment for Ischemia-Reperfusion Injury.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Troponin I modulation of cardiac performance: Plasticity in the survival switch.Archives of biochemistry and biophysics · 2019Review
- A selective inhibitor of mitofusin 1-βIIPKC association improves heart failure outcome in rats.Nature communications · 2019Article
- Functional communication between PKC-targeted cardiac troponin I phosphorylation sites.Archives of biochemistry and biophysics · 2017Article
- Long-Term Biased β-Arrestin Signaling Improves Cardiac Structure and Function in Dilated Cardiomyopathy.Circulation · 2017Article
- Cardiac troponin structure-function and the influence of hypertrophic cardiomyopathy associated mutations on modulation of contractility.Archives of biochemistry and biophysics · 2016Review
- Functionally conservative substitutions at cardiac troponin I S43/45.Archives of biochemistry and biophysics · 2016Article
- TNNI1, TNNI2 and TNNI3: Evolution, regulation, and protein structure-function relationships.Gene · 2016Review
- Gene regulation, alternative splicing, and posttranslational modification of troponin subunits in cardiac development and adaptation: a focused review.Frontiers in physiology · 2014Review
- Article
- Cardiac muscle activation blunted by a mutation to the regulatory component, troponin T.The Journal of biological chemistry · 2013Article
- Tropomyosin Ser-283 pseudo-phosphorylation slows myofibril relaxation.Archives of biochemistry and biophysics · 2013Article
- Post-translational modifications of myofilament proteins involved in length-dependent prolongation of relaxation in rabbit right ventricular myocardium.Archives of biochemistry and biophysics · 2013Article
- Inherited cardiomyopathies caused by troponin mutations.Journal of geriatric cardiology : JGC · 2013Article
- Oxidative stress and sarcomeric proteins.Circulation research · 2013Review
- Impact of site-specific phosphorylation of protein kinase A sites Ser23 and Ser24 of cardiac troponin I in human cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2013Article
- Tropomyosin dephosphorylation results in compensated cardiac hypertrophy.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
There is evidence for PKC-dependent multisite phosphorylation of cardiac troponin I (cTnI) at Ser-23 and Ser-24 (also PKA sites) in the cardiac-specific N-terminal extension and at Thr-144, a unique residue in the inhibitory region. The functional effect of these phosphorylations in combination is of interest in view of data indicating intramolecular interaction between the N-terminal extension and the inhibitory region of cTnI. To determine the role of PKC-dependent phosphorylation of cTnI on sarcomeric function, we measured contractile regulation at multiple levels of complexity. Ca(2+) binding to thin filaments reconstituted with either cTnI(wild-type) or pseudo-phosphorylated cTnI(S23D/S24D), cTnI(T144E), and cTnI(S23D/S24D/T144E) was determined. Compared with controls regulated by cTnI(wild-type), thin filaments with cTnI(S23D/S24D) and cTnI(S23D/S24D/T144E) exhibited decreased Ca(2+) sensitivity. In contrast, there was no significant difference between Ca(2+) binding to thin filaments with cTnI(wild-type) and with cTnI(T144E). Studies of the pCa-force relations in skinned papillary fibers regulated by these forms of cTnI yielded similar results. However, in both the Ca(2+) binding measurements and the skinned fiber tension measurements, the presence of cTnI(S23D/S24D/T144E) induced a much lower Hill coefficient than either wild type, S23D/S24D, or T144E. These data highlight the importance of thin filament-based cooperative mechanisms in cardiac regulation, with implications for mechanisms of control of function in normal and pathological hearts.
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