ArticleBiochemistry2006
Selective deletion of the NH2-terminal variable region of cardiac troponin T in ischemia reperfusion by myofibril-associated mu-calpain cleavage.
Article in Biochemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 93 citations in OpenAlex.
- Thin filament interaction and CaJournal of molecular and cellular cardiology · 2026Article
- The highly conserved C-terminal end segment of troponin T binds tropomyosin and actin to function in modulating contractile kinetics.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Role of the interaction between troponin T and AMP deaminase by zinc bridge in modulating muscle contraction and ammonia production.Molecular and cellular biochemistry · 2024Review
- The roles of intracellular proteolysis in cardiac ischemia-reperfusion injury.Basic research in cardiology · 2023Review
- Reversing mitochondrial defects in aged hearts: role of mitochondrial calpain activation.American journal of physiology. Cell physiology · 2022Article
- Monoclonal Antibodies as Probes to Study Ligand-Induced Conformations of Troponin Subunits.Frontiers in physiology · 2022Article
- Cardiac Troponin T: The Impact of Posttranslational Modifications on Analytical Immunoreactivity in Blood up to the Excretion in Urine.Advances in experimental medicine and biology · 2021Article
- NHJournal of cellular signaling · 2021Article
- Calpain-2 participates in the process of calpain-1 inactivation.Bioscience reports · 2020Article
- Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse.International journal of molecular sciences · 2020Review
- The evolutionarily conserved C-terminal peptide of troponin I is an independently configured regulatory structure to function as a myofilament CaJournal of molecular and cellular cardiology · 2019Article
- Multi-Site Coronary Vein Sampling Study on Cardiac Troponin T Degradation in Non-ST-Segment-Elevation Myocardial Infarction: Toward a More Specific Cardiac Troponin T Assay.Journal of the American Heart Association · 2019Article
- SMYD2 glutathionylation contributes to degradation of sarcomeric proteins.Nature communications · 2018Article
- Role of the HPRG Component of Striated Muscle AMP Deaminase in the Stability and Cellular Behaviour of the Enzyme.Biomolecules · 2018Review
- Will you still need me (CaAging cell · 2017Article
- Increases of desmin and α-actinin in mouse cardiac myofibrils as a response to diastolic dysfunction.Journal of molecular and cellular cardiology · 2016Article
- TNNT1, TNNT2, and TNNT3: Isoform genes, regulation, and structure-function relationships.Gene · 2016Review
- Protein Structure-Function Relationship at Work: Learning from Myopathy Mutations of the Slow Skeletal Muscle Isoform of Troponin T.Frontiers in physiology · 2016Review
- Cardioprotection in ischaemia-reperfusion injury: novel mechanisms and clinical translation.The Journal of physiology · 2015Review
- NH2-terminal truncations of cardiac troponin I and cardiac troponin T produce distinct effects on contractility and calcium homeostasis in adult cardiomyocytes.American journal of physiology. Cell physiology · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The structure of the NH2-terminal region of troponin T (TnT) is hypervariable among the muscle type-specific isoforms and is also regulated by alternative RNA splicing. This region does not contain binding sites for other thin filament proteins, but alteration of its structure affects the Ca2+ regulation of muscle contraction. Here we report a truncated cardiac TnT produced during myocardial ischemia reperfusion. Amino acid sequencing and protein fragment reconstruction determined that it is generated by a posttranslational modification selectively removing the NH2-terminal variable region and preserving the conserved core structure of TnT. Triton X-100 extraction of cardiac muscle fibers promoted production of the NH2-terminal truncated cardiac TnT (cTnT-ND), indicating a myofibril-associated proteolytic activity. Mu-calpain is a myofibril-associated protease and is known to degrade TnT. Supporting a role of mu-calpain in producing cTnT-ND in myocardial ischemia reperfusion, calpain inhibitors decreased the level of cTnT-ND in Triton-extracted myofibrils. Mu-calpain treatment of the cardiac myofibril and troponin complex specifically reproduced cTnT-ND. In contrast, mu-calpain treatment of isolated cardiac TnT resulted in nonspecific degradation, suggesting that this structural modification is relevant to physiological structures of the myofilament. Triton X-100 treatment of transgenic mouse cardiac myofibrils overexpressing fast skeletal muscle TnT produced similar NH2-terminal truncations of the endogenous and exogenous TnT, despite different amino acid sequences at the cleavage site. With the functional consequences of removing the NH2-terminal variable region of TnT, the mu-calpain-mediated proteolytic modification of TnT may act as an acute mechanism to adjust muscle contractility under stress conditions.
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