ArticleAmerican journal of physiology. Cell physiology2008
Adaptation by alternative RNA splicing of slow troponin T isoforms in type 1 but not type 2 Charcot-Marie-Tooth disease.
Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- FSHD muscle shows perturbation in fibroadipogenic progenitor cells, mitochondrial function and alternative splicing independently of inflammation.Human molecular genetics · 2024Pooled it
- Troponin: biology, molecular mechanisms, and multidimensional clinical applications.Molecular biomedicine · 2026Review
- A homozygous single-nucleotide variant inJournal of neuromuscular diseases · 2025Article
- Congenital myopathies: pathophysiological mechanisms and promising therapies.Journal of translational medicine · 2024Review
- Troponin Variants as Markers of Skeletal Muscle Health and Diseases.Frontiers in physiology · 2021Review
- Novel Recessive TNNT1 Congenital Core-Rod Myopathy in French Canadians.Annals of neurology · 2020Article
- 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
- Novel autosomal dominant TNNT1 mutation causing nemaline myopathy.Molecular genetics & genomic medicine · 2017Article
- 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
- Human slow troponin T (TNNT1) pre-mRNA alternative splicing is an indicator of skeletal muscle response to resistance exercise in older adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2014Article
- Deficiency of slow skeletal muscle troponin T causes atrophy of type I slow fibres and decreases tolerance to fatigue.The Journal of physiology · 2014Article
- The functional properties of human slow skeletal troponin T isoforms in cardiac muscle regulation.The Journal of biological chemistry · 2012Article
- Structure of the NH2-terminal variable region of cardiac troponin T determines its sensitivity to restrictive cleavage in pathophysiological adaptation.Archives of biochemistry and biophysics · 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
7 authors at 5 institutions in 3 countries.
Funding
Abstract
Slow troponin T (TnT) plays an indispensable role in skeletal muscle function. Alternative RNA splicing in the NH(2)-terminal region produces high-molecular-weight (HMW) and low-molecular-weight (LMW) isoforms of slow TnT. Normal adult slow muscle fibers express mainly HMW slow TnT. Charcot-Marie-Tooth disease (CMT) is a group of inherited peripheral polyneuropathies caused by various neuronal defects. We found in the present study that LMW slow TnT was significantly upregulated in demyelination form type 1 CMT (CMT1) but not axonal form type 2 CMT (CMT2) muscles. Contractility analysis showed an increased specific force in single fibers isolated from CMT1 but not CMT2 muscles compared with control muscles. However, an in vitro motility assay showed normal velocity of the myosin motor isolated from CMT1 and CMT2 muscle biopsies, consistent with their unchanged myosin isoform contents. Supporting a role of slow TnT isoform regulation in contractility change, LMW and HMW slow TnT isoforms showed differences in the molecular conformation in conserved central and COOH-terminal regions with changed binding affinity for troponin I and tropomyosin. In addition to providing a biochemical marker for the differential diagnosis of CMT, the upregulation of LMW slow TnT isoforms under the distinct pathophysiology of CMT1 demonstrates an adaptation of muscle function to neurological disorders by alternative splicing modification of myofilament proteins.
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