ArticleThe Journal of clinical investigation1996
Altered cardiac troponin T in vitro function in the presence of a mutation implicated in familial hypertrophic cardiomyopathy.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 118 citations in OpenAlex.
- Cardiac troponin T (TNNT2) mutations in chinese dilated cardiomyopathy patients.BioMed research international · 2014Trial
- Motility Assay to Probe the Calcium Sensitivity of Myosin and Regulated Thin Filaments.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Cardiac troponin T N-domain variant destabilizes the actin interface resulting in disturbed myofilament function.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- High-resolution cryo-EM structure of the junction region of the native cardiac thin filament in relaxed state.PNAS nexus · 2023Article
- A novel nonsense mutation in TNNT2 in a Chinese pedigree with hypertrophic cardiomyopathy: A case report.Medicine · 2020Article
- TNNT1, TNNT2, and TNNT3: Isoform genes, regulation, and structure-function relationships.Gene · 2016Review
- Effects of hypertrophic and dilated cardiomyopathy mutations on power output by human β-cardiac myosin.The Journal of experimental biology · 2016Review
- Clinical phenotype and outcome of hypertrophic cardiomyopathy associated with thin-filament gene mutations.Journal of the American College of Cardiology · 2014Article
- Allosteric effects of cardiac troponin TNT1 mutations on actomyosin binding: a novel pathogenic mechanism for hypertrophic cardiomyopathy.Archives of biochemistry and biophysics · 2014Article
- A Drosophila melanogaster model of diastolic dysfunction and cardiomyopathy based on impaired troponin-T function.Circulation research · 2014Article
- Analysis of the molecular pathogenesis of cardiomyopathy-causing cTnT mutants I79N, ΔE96, and ΔK210.Biophysical journal · 2013Article
- Article
- Thin filament mutations: developing an integrative approach to a complex disorder.Circulation research · 2011Review
- Facilitated cross-bridge interactions with thin filaments by familial hypertrophic cardiomyopathy mutations in α-tropomyosin.Journal of biomedicine & biotechnology · 2011Article
- Dual regulatory functions of the thin filament revealed by replacement of the troponin I inhibitory peptide with a linker.The Journal of biological chemistry · 2010Article
- Mechanical and energetic consequences of HCM-causing mutations.Journal of cardiovascular translational research · 2009Review
- Sarcomeric proteins and familial hypertrophic cardiomyopathy: linking mutations in structural proteins to complex cardiovascular phenotypes.Heart failure reviews · 2005Review
- Expression of slow skeletal myosin binding C-protein in normal adult mammalian heart.Journal of muscle research and cell motility · 2005Article
- The Delta 14 mutation of human cardiac troponin T enhances ATPase activity and alters the cooperative binding of S1-ADP to regulated actin.Biochemistry · 2004Article
- Structural based insights into the role of troponin in cardiac muscle pathophysiology.Journal of muscle research and cell motility · 2004Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Familial hypertrophic cardiomyopathy (HCM) can be caused by dominant missense mutations in cardiac troponin T (TnT), alpha-tropomyosin, C-protein, or cardiac myosin heavy chain genes. The myosin mutations are known to impair function, but any functional consequences of the TnT mutations are unknown. This report describes the in vitro function of troponin containing an IIe91Asn mutation in rat cardiac TnT, corresponding to the HCM-causing Ile79Asn mutation in man. Mutant and wild-type TnT cDNAs were expressed in bacteria and the proteins purified and reconstituted with the other troponin subunits, the mutation had no effect on troponin's affinity for tropomyosin, troponin-induced binding of tropomyosin to actin, cooperative binding of myosin subfragment 1 to the thin filament, CA(2+)-sensitive regulation of thin filament-myosin subfragment 1 ATPase activity, or the CA2+ concentration dependence of this regulation. However, the mutation resulted in 50% faster thin filament movement over a surface coated with heavy meromyosin in in vitro motility assays. The increased sliding speed suggests an unexpected role for the amino terminal region of TnT in which this mutation occurs. The relationship between this faster motility and altered cardiac contraction in patients with HCM is discussed.
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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.