ReviewComprehensive Physiology2018
Thick Filament Protein Network, Functions, and Disease Association.
Review in Comprehensive Physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed, 72 citations in OpenAlex.
- Four New Muscle Myosin II Binding Properties of Titin: Implications for Myofibrillogenesis.Cytoskeleton (Hoboken, N.J.) · 2026Article
- Unbiased cleavage site prediction uncovers viral antagonism of host innate immunity by SARS-CoV-2 3C-like protease.JCI insight · 2026Article
- Novel GJC2 and OBSCN variants co-segregating in a Chinese primary lymphedema pedigree.Orphanet journal of rare diseases · 2026Article
- Annotating the x-ray diffraction pattern of vertebrate striated muscle.Biophysical journal · 2025Article
- Sex-dependent and muscle-specific progression of the MYBPC1 E248K Myotrem myopathy in response to aging.JCI insight · 2025Article
- New Types of Post-Translational Modification of Proteins in Cardiovascular Diseases.Journal of cardiovascular translational research · 2025Review
- MYL1-Related Congenital Myopathy: Clinical, Genetic and Pathological Insights.Neuropathology and applied neurobiology · 2025Article
- Disparate Molecular Properties of Two Hypertrophic Cardiomyopathy-Associated cMyBP-C Mutants Reveal Distinct Pathogenic Mechanisms Beyond Haploinsufficiency.Biomedicines · 2025Article
- Constitutive deletion of the obscurin-Ig58/59 domains induces atrial remodeling and Ca2+-based arrhythmogenesis.JCI insight · 2025Article
- Hyperpolarized-MRI in Hypertrophic Cardiomyopathy: A Narrative Review.Clinical Medicine Insights. Cardiology · 2025Review
- An integrated picture of the structural pathways controlling the heart performance.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Post-translational modifications of vertebrate striated muscle myosin heavy chains.Cytoskeleton (Hoboken, N.J.) · 2024Review
- Muscle Proteome Analysis of Facioscapulohumeral Dystrophy Patients Reveals a Metabolic Rewiring Promoting Oxidative/Reductive Stress Contributing to the Loss of Muscle Function.Antioxidants (Basel, Switzerland) · 2024Article
- Essential role of obscurin kinase-1 in cardiomyocyte coupling via N-cadherin phosphorylation.JCI insight · 2024Article
- Obscurin Maintains Myofiber Identity in Extraocular Muscles.Investigative ophthalmology & visual science · 2024Article
- Missense mutations in the central domains of cardiac myosin binding protein-C and their potential contribution to hypertrophic cardiomyopathy.The Journal of biological chemistry · 2024Article
- Comprehensive somatic mutational analysis in glioblastoma: Implications for precision medicine approaches.PloS one · 2024Article
- A Case of a Patient WithTremor and other hyperkinetic movements (New York, N.Y.) · 2024Article
- Article
- α-myosin heavy chain lactylation maintains sarcomeric structure and function and alleviates the development of heart failure.Cell research · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Sarcomeres consist of highly ordered arrays of thick myosin and thin actin filaments along with accessory proteins. Thick filaments occupy the center of sarcomeres where they partially overlap with thin filaments. The sliding of thick filaments past thin filaments is a highly regulated process that occurs in an ATP-dependent manner driving muscle contraction. In addition to myosin that makes up the backbone of the thick filament, four other proteins which are intimately bound to the thick filament, myosin binding protein-C, titin, myomesin, and obscurin play important structural and regulatory roles. Consistent with this, mutations in the respective genes have been associated with idiopathic and congenital forms of skeletal and cardiac myopathies. In this review, we aim to summarize our current knowledge on the molecular structure, subcellular localization, interacting partners, function, modulation via posttranslational modifications, and disease involvement of these five major proteins that comprise the thick filament of striated muscle cells. © 2018 American Physiological Society. Compr Physiol 8:631-709, 2018.
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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 Socratic graph.