ReviewJournal of muscle research and cell motility2011
The 3-state model of muscle regulation revisited: is a fourth state involved?
Review in Journal of muscle research and cell motility, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 31 citations in OpenAlex.
- C-terminal troponin-I residues trap tropomyosin in the muscle thin filament blocked-state.Biochemical and biophysical research communications · 2021Article
- Cryo-EM and Molecular Docking Shows Myosin Loop 4 Contacts Actin and Tropomyosin on Thin Filaments.Biophysical journal · 2020Article
- A role for actin flexibility in thin filament-mediated contractile regulation and myopathy.Nature communications · 2020Article
- A new twist on tropomyosin binding to actin filaments: perspectives on thin filament function, assembly and biomechanics.Journal of muscle research and cell motility · 2020Review
- Thin filament dysfunctions caused by mutations in tropomyosin Tpm3.12 and Tpm1.1.Journal of muscle research and cell motility · 2020Review
- Modeling and simulation of excitation- contraction coupling of fast-twitch skeletal muscle fibers.Technology and health care : official journal of the European Society for Engineering and Medicine · 2020Article
- Sarcomere length-dependent effects on CaThe Journal of general physiology · 2019Article
- CaBiophysical journal · 2018Article
- Role of the C-terminus mobile domain of cardiac troponin I in the regulation of thin filament activation in skinned papillary muscle strips.Archives of biochemistry and biophysics · 2018Article
- Heart Failure-Related Hyperphosphorylation in the Cardiac Troponin I C Terminus Has Divergent Effects on Cardiac Function In Vivo.Circulation. Heart failure · 2017Article
- Structural determinants of muscle thin filament cooperativity.Archives of biochemistry and biophysics · 2016Review
- Impact of tropomyosin isoform composition on fast skeletal muscle thin filament regulation and force development.Journal of muscle research and cell motility · 2015Article
- Poorly understood aspects of striated muscle contraction.BioMed research international · 2015Review
- In situ time-resolved FRET reveals effects of sarcomere length on cardiac thin-filament activation.Biophysical journal · 2014Article
- Cross-talk, cross-bridges, and calcium activation of cardiac contraction.Biophysical journal · 2014Article
- The myosin-activated thin filament regulatory state, M⁻-open: a link to hypertrophic cardiomyopathy (HCM).Journal of muscle research and cell motility · 2014Review
- Hypertrophic cardiomyopathy: how do mutations lead to disease?Arquivos brasileiros de cardiologia · 2014Review
- Structural basis for the in situ Ca(2+) sensitization of cardiac troponin C by positive feedback from force-generating myosin cross-bridges.Archives of biochemistry and biophysics · 2013Article
- Structural and kinetic effects of hypertrophic cardiomyopathy related mutations R146G/Q and R163W on the regulatory switching activity of rat cardiac troponin I.Archives of biochemistry and biophysics · 2013Article
- Potentiation in mouse lumbrical muscle without myosin light chain phosphorylation: is resting calcium responsible?The Journal of general physiology · 2013Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The 3-state model of muscle regulation has been useful in explaining the roles of Ca2+ and myosin heads in activation and relaxation of striated muscle contraction. However, there are some phenomena, which cannot simply be explained by the 3-state model. These include increased Ca2+-binding caused by strong-binding myosin heads and residual active force at low Ca2+ in the case of familial hypertrophic cardiomyopathy. Here, I review experimental data which provide evidence for an additional state, a myosin-induced Open state present in the absence of Ca2+ (Open-Ca2+) which like the normal Open+Ca2+ state, is an active state and can allow myosin heads to cycle and generate force. A schematic diagram is presented which shows that the formation of the Open-Ca2+ state is on a parallel path with the formation of the Open+Ca2+ state and can contribute to activation.
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What OpenQuestion holds
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.