ArticleBiochemical and biophysical research communications2011
Several cardiomyopathy causing mutations on tropomyosin either destabilize the active state of actomyosin or alter the binding properties of tropomyosin.
Article in Biochemical and biophysical research communications, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Creatine Kinase Equilibration and ΔGInternational journal of molecular sciences · 2023Article
- Thin filament cardiomyopathies: A review of genetics, disease mechanisms, and emerging therapeutics.Frontiers in cardiovascular medicine · 2022Review
- Computational and biophysical determination of pathogenicity of variants of unknown significance in cardiac thin filament.JCI insight · 2021Article
- Thin filament dysfunctions caused by mutations in tropomyosin Tpm3.12 and Tpm1.1.Journal of muscle research and cell motility · 2020Review
- A Stochastic Multiscale Model of Cardiac Thin Filament Activation Using Brownian-Langevin Dynamics.Biophysical journal · 2019Article
- Cardiomyopathy-associated mutations in tropomyosin differently affect actin-myosin interaction at single-molecule and ensemble levels.Journal of muscle research and cell motility · 2019Review
- Effects of cardiomyopathy-linked mutations K15N and R21H in tropomyosin on thin-filament regulation and pointed-end dynamics.Molecular biology of the cell · 2019Article
- Stepwise C-Terminal Truncation of Cardiac Troponin T Alters Function at Low and Saturating CaBiophysical journal · 2018Article
- Transmission of stability information through the N-domain of tropomyosin is interrupted by a stabilizing mutation (A109L) in the hydrophobic core of the stability control region (residues 97-118).The Journal of biological chemistry · 2014Article
- Nuclear tropomyosin and troponin in striated muscle: new roles in a new locale?Journal of muscle research and cell motility · 2013Review
- A study of tropomyosin's role in cardiac function and disease using thin-filament reconstituted myocardium.Journal of muscle research and cell motility · 2013Review
- Slowed Dynamics of Thin Filament Regulatory Units Reduces CaCellular and molecular bioengineering · 2013Article
- α-Tropomyosin with a D175N or E180G mutation in only one chain differs from tropomyosin with mutations in both chains.Biochemistry · 2012Article
- Disease causing mutations of troponin alter regulated actin state distributions.Journal of muscle research and cell motility · 2012Review
- Congenital myopathy-causing tropomyosin mutations induce thin filament dysfunction via distinct physiological mechanisms.Human molecular genetics · 2012Article
- Familial hypertrophic cardiomyopathy related E180G mutation increases flexibility of human cardiac α-tropomyosin.FEBS letters · 2012Article
- Persistence length of human cardiac α-tropomyosin measured by single molecule direct probe microscopy.PloS one · 2012Article
- Tropomyosin flexural rigidity and single ca(2+) regulatory unit dynamics: implications for cooperative regulation of cardiac muscle contraction and cardiomyocyte hypertrophy.Frontiers in physiology · 2012Article
- Micromechanical thermal assays of Ca2+-regulated thin-filament function and modulation by hypertrophic cardiomyopathy mutants of human cardiac troponin.Journal of biomedicine & biotechnology · 2012Article
- Detection of target ssDNA using a microfabricated Hall magnetometer with correlated optical readout.Journal of biomedicine & biotechnology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We examined the cardiomyopathy-causing tropomyosin mutations E180G, D175N, and V95A to determine their effects on actomyosin regulation. V95A reduced the ATPase rate when filaments were saturated with regulatory proteins both in the presence and absence of calcium, indicating either a stabilization of the inactive state or an inability to fully populate the active state. Effects of E180G and D175N were more complex. These two mutations increased ATPase rates at sub-saturating concentrations of troponin and tropomyosin as compared to wild type tropomyosin. At higher concentrations of regulatory proteins, ATPase rates became similar to wild type. Normal activation was achieved with the tight-binding myosin analog N-ethylmaleimide-S1, at saturating regulatory protein concentrations. These results suggest that the E180G and D175N mutations reduce the affinity of tropomyosin for actin and also destabilize troponin binding to the actin thin filaments.
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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.