ReviewJournal of muscle research and cell motility2014
The myosin-activated thin filament regulatory state, M⁻-open: a link to hypertrophic cardiomyopathy (HCM).
Review in Journal of muscle research and cell motility, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Hypertrophic Cardiomyopathy Mutations of Troponin Reveal Details of Striated Muscle Regulation.Frontiers in physiology · 2022Pooled it
- Modeling the effects of thin filament near-neighbor cooperative interactions in mammalian myocardium.The Journal of general physiology · 2025Article
- Dilated Cardiomyopathy - Exploring the Underlying Causes.Medical research archives · 2024Article
- Cooperative mechanisms underlie differences in myocardial contractile dynamics between large and small mammals.The Journal of general physiology · 2023Article
- Novel Mutation Glu98Lys in Cardiac Tropomyosin Alters Its Structure and Impairs Myocardial Relaxation.International journal of molecular sciences · 2023Article
- De Novo Asp219Val Mutation in Cardiac Tropomyosin Associated with Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2022Article
- Generative adversarial networks for construction of virtual populations of mechanistic models: simulations to study Omecamtiv Mecarbil action.Journal of pharmacokinetics and pharmacodynamics · 2022Article
- Eliminating the First Inactive State and Stabilizing the Active State of the Cardiac Regulatory System Alters Behavior in Solution and in Ordered Systems.Biochemistry · 2020Article
- The molecular basis for diminished muscle function in acidosis: a proposal.Journal of muscle research and cell motility · 2020Article
- Muscle Cell Morphogenesis, Structure, Development and Differentiation Processes Are Significantly Regulated during Human Ovarian Granulosa Cells In Vitro Cultivation.Journal of clinical medicine · 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
- The mechanism of thin filament regulation: Models in conflict?The Journal of general physiology · 2019Review
- Sarcomere length-dependent effects on CaThe Journal of general physiology · 2019Article
- The Relaxation Properties of Myofibrils Are Compromised by Amino Acids that Stabilize α-Tropomyosin.Biophysical journal · 2017Article
- Order-Disorder Transitions in the Cardiac Troponin Complex.Journal of molecular biology · 2016Review
- Structural determinants of muscle thin filament cooperativity.Archives of biochemistry and biophysics · 2016Review
- The cMyBP-C HCM variant L348P enhances thin filament activation through an increased shift in tropomyosin position.Journal of molecular and cellular cardiology · 2016Article
- Contributions of Ca2+-Independent Thin Filament Activation to Cardiac Muscle Function.Biophysical journal · 2015Article
- N-acetylcysteine reverses diastolic dysfunction and hypertrophy in familial hypertrophic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
This review proposes a link between the hypertrophic (HCM) and restrictive cardiomyopathies caused by mutations in several sarcomeric thin filament proteins, and the open state of the three-state muscle regulation theory. The three characteristics of various muscle systems reconstituted from HCM mutated proteins (increased Ca(2+)-sensitivity, increased basal activity in the absence of Ca(2+), and decreased cooperativity) can be explained by the contribution of a myosin-induced open state (M (-) ), which elevates the basal activity and competes with the normal Ca(2+)-activated pathway. A model based on the three-state theory of regulation, shows how a change in the closed/blocked equilibrium caused by a mutation that weakens the binding of troponin I to tropomyosin-actin can produce the characteristics of HCM. This review also shows that in the M (-) state, Ca(2+) can shift the closed-open equilibrium of the N-terminal hydrophobic region of troponin C without affecting activity.
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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.