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MYL3 Regulatory light chain of myosin. Does not bind calcium. Defects in MYL3 are the cause of familial hypertrophic cardiomyopathy type 8 (CMH8). Familial hypertrophic cardiomyopathy is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death. CMH8 inheritance can be autosomal dominant or recessive. Note: This description may include information from UniProtKB.
Protein type: Motility/polarity/chemotaxis; Motor
Chromosomal Location of Human Ortholog: 3p21.31
Cellular Component: A band; cytosol; I band; muscle myosin complex; sarcomere
Molecular Function: actin monomer binding; calcium ion binding; motor activity; myosin II heavy chain binding; structural constituent of muscle
Biological Process: cardiac muscle contraction; muscle filament sliding; positive regulation of ATPase activity; regulation of striated muscle contraction; regulation of the force of heart contraction; skeletal muscle tissue development; ventricular cardiac muscle tissue morphogenesis
Disease: Cardiomyopathy, Familial Hypertrophic, 8
Reference #:  P08590 (UniProtKB)
Alt. Names/Synonyms: Cardiac myosin light chain 1; CMH8; CMLC1; MLC1SB; MLC1V; MYL3; Myosin light chain 1, slow-twitch muscle B/ventricular isoform; Myosin light chain 3; myosin, light chain 3, alkali; myosin, light polypeptide 3, alkali; ventricular, skeletal, slow; Ventricular/slow twitch myosin alkali light chain; VLC1
Gene Symbols: MYL3
Molecular weight: 21,932 Da
Basal Isoelectric point: 5.03  Predict pI for various phosphorylation states
CST Pathways:  Actin Dynamics
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Protein Structure Not Found.
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