ArticleAmerican journal of physiology. Heart and circulatory physiology2009
Nonmyofilament-associated troponin T fragments induce apoptosis.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Potential cytotoxicity of truncated slow skeletal muscle troponin T (ssTnT) in a loss of function TNNT1 myopathy mouse model.The FEBS journal · 2025Article
- Non-Canonical Localization of Cardiac Troponins: Expanding Functions or Causing Pathologies?International journal of molecular sciences · 2024Review
- Cardiac troponin T and autoimmunity in skeletal muscle aging.GeroScience · 2022Article
- The loss of slow skeletal muscle isoform of troponin T in spindle intrafusal fibres explains the pathophysiology of Amish nemaline myopathy.The Journal of physiology · 2019Article
- Troponin through the looking-glass: emerging roles beyond regulation of striated muscle contraction.Oncotarget · 2018Review
- 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
- Gene regulation, alternative splicing, and posttranslational modification of troponin subunits in cardiac development and adaptation: a focused review.Frontiers in physiology · 2014Review
- Troponin T nuclear localization and its role in aging skeletal muscle.Age (Dordrecht, Netherlands) · 2013Article
- Nonmyofilament-associated troponin T3 nuclear and nucleolar localization sequence and leucine zipper domain mediate muscle cell apoptosis.Cytoskeleton (Hoboken, N.J.) · 2013Article
- Pathogenic properties of the N-terminal region of cardiac myosin binding protein-C in vitro.Journal of muscle research and cell motility · 2012Article
- Preferential skeletal muscle myosin loss in response to mechanical silencing in a novel rat intensive care unit model: underlying mechanisms.The Journal of physiology · 2011Article
- Troponin T isoforms and posttranscriptional modifications: Evolution, regulation and function.Archives of biochemistry and biophysics · 2011Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Troponin T (TnT) is a striated muscle-specific protein and an abundant component of the myofilaments. Nonmyofilament-associated TnT is rapidly degraded in myocytes, implying an importance in the maintenance of the cellular environment. However, if the level of nonmyofilament-associated TnT or TnT fragments exceeds the degradation capacity, it may cause cytotoxicity. To investigate this hypothesis, we constructed bicistronic vectors to express different portions of TnT polypeptide chain, together with nonfusion green fluorescent protein as a tracer for the transfection. Cytotoxicity of the TnT fragments was studied through forced expression in C(2)C(12) myoblasts and human embryonic kidney-293 nonmuscle cells and examination of the viability of the transfected cells. The results demonstrated that, in the absence of myofilaments, the conserved COOH-terminal and middle fragments of TnT were highly effective on inducing cell death via apoptosis, whereas the NH(2)-terminal variable region was not. As combined effects, nonmyofilament-associated intact cardiac TnT and a COOH-terminal truncated slow TnT fragment found in Amish nemaline myopathy exhibited intermediate cytotoxicity. A particular significance of this finding is that peak releases of TnT or TnT fragments from decomposition of a large number of myofibrils in acute myocardial infarction may breach the cellular protection of proteolytic degradation and result in apoptosis as a potential cause for the loss of cardiomyocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.