ArticlePflugers Archiv : European journal of physiology2007
Functional effects of the DCM mutant Gly159Asp troponin C in skinned muscle fibres.
Article in Pflugers Archiv : European journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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
11 citing papers in PubMed, 21 citations in OpenAlex.
- Assessing Cardiac Contractility From Single Molecules to Whole Hearts.JACC. Basic to translational science · 2024Review
- Early sensitization of myofilaments to Ca2+ prevents genetically linked dilated cardiomyopathy in mice.Cardiovascular research · 2017Article
- Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling.Journal of visualized experiments : JoVE · 2016Article
- Review
- Myofilament dysfunction as an emerging mechanism of volume overload heart failure.Pflugers Archiv : European journal of physiology · 2014Review
- Biochemical characterisation of Troponin C mutations causing hypertrophic and dilated cardiomyopathies.Journal of muscle research and cell motility · 2014Review
- Significance of troponin dynamics for Ca2+-mediated regulation of contraction and inherited cardiomyopathy.The Journal of biological chemistry · 2012Article
- Thin filament mutations: developing an integrative approach to a complex disorder.Circulation research · 2011Review
- Article
- A novel mutant cardiac troponin C disrupts molecular motions critical for calcium binding affinity and cardiomyocyte contractility.Biophysical journal · 2008Article
- Force transients and minimum cross-bridge models in muscular contraction.Journal of muscle research and cell motility · 2007Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We recently reported a dilated cardiomyopathy (DCM) causing mutation in a novel disease gene, TNNC1, which encodes cardiac troponin C (TnC). We have determined how this mutation, Gly159Asp, affects contractile regulation when incorporated into muscle fibres. Endogenous troponin in rabbit skinned psoas fibres was partially replaced by recombinant human cardiac troponin containing either wild-type or Gly159Asp TnC. We measured both the force-pCa relationship of these fibres and the activation rate using the caged-Ca(2+) compound nitrophenyl-EGTA. Gly159Asp TnC had no significant effect on either the Ca(2+) sensitivity or cooperativity of force generation when compared to wild type. However, the mutation caused a highly significant (ca. 50%) decrease in the rate of activation. This study shows that whilst not affecting the force-pCa relationship, the mutation Gly159Asp causes a significant decrease in the rate of force production and a change in the relationship between the rate of force production and generated force. In vivo, this mutation may cause both a slowing of force generation and reduction in total systolic force. This represents a novel mechanism by which a cardiomyopathy-causing mutation can affect contractility.
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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.