Molecular Research on Muscle Protein and Myopathies
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biophysics".
Deadline for manuscript submissions: closed (29 July 2021) | Viewed by 33634
Special Issue Editors
Interests: congenital myopathy; molecular mechanisms of muscle contraction; muscle proteins; polarized microfluorimetry
Special Issues, Collections and Topics in MDPI journals
Interests: congenital myopathies; mutations of tropomyosin; thin filament regulation; conformational rearrangements of contractile proteins; actin-myosin interaction; myosin ATPase activity; contractile dysfunction; therapeutic approaches
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Muscle contraction is based on the cyclic interaction between actin and myosin, accompanied by ATP hydrolysis in the active center of the myosin motor domain. As a result of this interaction, the myosin filaments slide relative to the actin filaments, and the muscle sarcomeres shorten. Disruption of the molecular mechanisms of actin–myosin regulation in cardiac and skeletal muscles due to mutations in muscle proteins genes is causative of severe diseases—hereditary myopathies—which have an extremely negative effect on the quality of human life. Understanding the primary causes of muscle weakness and hypotension in cardiac and skeletal muscles in hereditary myopathies is necessary for early diagnosis and prognosis of the disease and for the development of therapeutic approaches to restore muscle contractile function. The purpose of this Special Issue is to summarize new data on the functional consequences of mutant toxic proteins for the sarcomere, to elucidate the relationship between mutations and disease phenotypes, and to identify targets for action in order to correct dysfunctions in various myopathies.
Authors are invited to contribute to this Special Issue, which will publish priority studies clarifying the molecular mechanisms of dysfunctions in cardiac and skeletal myopathies.
Topics include, but are not limited to:
- study of structural and functional consequences of amino acid substitutions and deletions in sarcomeric proteins (actin, myosin, tropomyosin, troponin, nebulin, cofilin) associated with various variants of myopathies;
- identification of impaired protein–protein interactions in the presence of mutations in sarcomeric proteins and analysis of further pathways of contractile dysfunction in cardiac and skeletal myopathies;
- identification of targets for the restoration of normal muscle function;
- search and testing of potential drugs for the treatment of muscle dysfunctions.
Dr. Yurii Borovikov
Prof. Dr. Yurii Borovikov
Guest Editors
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Keywords
- congenital skeletal myopathy
- cardiomyopathy
- desease-causing mutations
- muscle contraction
- calcium regulation
- cross-bridge cycling and kinetics
- thin filament
- ATPase activity
- actin–myosin interaction
- therapeutic approaches
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