Abstract
Myosin is an essential driver of cardiac and skeletal muscle function. Multiple mutations identified in β-cardiac/skeletal slow myosin heavy chain (MYH7) and skeletal fast myosin heavy chain 2A (MYH2), cause a group of human skeletal muscle diseases termed myosinopathies. Over 90% of these mutations are found in the filament-forming region of the coiled-coil tail, also known as light meromyosin (LMM). Mutation to a proline residue or deletion of a single residue are common. Both are predicted to strongly affect the secondary structure of the coiled coil, and by extension their incorporation into the thick filament.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
