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The beta-myosin heavy chain (MYH7) protein is a crucial component of muscle fibers, particularly in cardiac muscle. Encoded by the MYH7 gene located on chromosome 14q11.2, MYH7 contains 1,938 amino acids with a molecular weight of around 223 kDa. Post-translational modifications of MYH7 include phosphorylation, glycosylation, and disulfide bond formation, which regulate its function and interactions with other proteins. MYH7 is primarily an intracellular protein, forming part of the thick filaments in sarcomeres, the basic contractile units of muscle cells.
The main function of MYH7 is to generate force and power during muscle contraction, particularly in the myocardium of the heart. It interacts with other proteins, such as actin and ATP, to convert chemical energy into mechanical work, enabling the heart to pump blood efficiently throughout the body. MYH7 is predominantly expressed in cardiac muscle cells (cardiomyocytes), where it plays a central role in cardiac contraction and relaxation.
Expression of MYH7 is tightly regulated at transcriptional, translational, and post-translational levels, influenced by various factors, including developmental cues, hormonal signals, and mechanical stress on the heart. For example, the activity of transcription factors such as GATA4 and serum response factor (SRF) can modulate MYH7 expression in response to changes in cardiac workload or pathological stimuli.
Mutations in the MYH7 gene have been associated with a range of cardiac disorders, including hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), and restrictive cardiomyopathy (RCM). HCM, in particular, is commonly linked to mutations in MYH7 and is characterized by abnormal thickening of the heart muscle, leading to impaired cardiac function and increased risk of arrhythmias and sudden cardiac death. These mutations often alter the structure or function of MYH7, affecting its contractile properties and leading to pathological changes in cardiac muscle.
While not targeting MYH7 directly, some researchers have disrupted downstream pathways associated with MYH7 dysfunction, which may hold promise for treating cardiac disorders such as HCM. Examples include therapies aimed at modulating calcium handling, myofilament sensitivity, or sarcomere function, which could mitigate the effects of MYH7 mutations and improve cardiac function in affected individuals.
MYH7 expression levels and mutations have been explored as potential markers for diagnostic and prognostic purposes in cardiac disorders. Detection of MYH7 mutations through genetic testing can aid in diagnosing inherited cardiomyopathies and guide clinical management strategies. Additionally, MYH7 expression patterns or levels in cardiac tissue may provide valuable insights into disease severity, progression, and response to therapy, serving as prognostic indicators for patient outcomes.
NeoBiotechnologies offers several antibodies against MYH7 that have been validated for immunohistochemistry. Additionally, we hold exclusive rights to MYH7 antibodies available for licensing or collaboration [https://www.neobiotechnologies.com/shop/?s=MYH7].
Myosin-7, Myosin heavy chain 7, Myosin heavy chain slow isoform, Myosin heavy chain, cardiac muscle beta isoform, Beta myosin heavy chain; cardiac muscle beta isoform; CMD1S; CMH1; MPD1; MyHC-beta; MyHC-slow; MYHCB; Myopathy, distal 1; Myosin heavy chain (AA 1-96); Myosin heavy chain slow isoform; Myosin heavy chain, cardiac muscle beta isoform; Myosin, heavy chain 7, cardiac muscle, beta; Myosin, heavy polypeptide 7, cardiac muscle, beta; Myosin-7; Rhabdomyosarcoma antigen MU RMS 40.7A; SPMD; SPMM
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