|Calculated MW||19794 Da|
|Other Names||Myosin regulatory light chain 12A, Epididymis secretory protein Li 24, HEL-S-24, MLC-2B, Myosin RLC, Myosin regulatory light chain 2, nonsarcomeric, Myosin regulatory light chain MRLC3, MYL12A, MLCB, MRLC3, RLC|
|Target/Specificity||A synthetic peptide corresponding to residues near the N-terminus of human Myosin RLC was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Myosin RLC Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||MLCB, MRLC3, RLC|
|Function||Myosin regulatory subunit that plays an important role in regulation of both smooth muscle and nonmuscle cell contractile activity via its phosphorylation. Implicated in cytokinesis, receptor capping, and cell locomotion (By similarity).|
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Provided below are standard protocols that you may find useful for product applications.
The muscle myosins and hexomeric proteins consisting of two heavy chains and two pairs of light chains, the latter called essential (ELC) and regulatory (RLC). The light chains stabilize the long alpha helical neck of the myosin head (1). Human myosin light chain-2 (MYL2) is an important protein involved in the regulation of myosin ATPase activity in smooth muscle. In cardiac muscle, the precise role of MYL2 is not well understood; however, an increase in ventricular MYL2 is observed during myocardial hypertrophy in cardiac patients with valve stenosis (2). Familial hypertrophic cardiomyopathy (FHC) is an autosomal dominant disease caused by mutations in all of the major sarcomeric proteins, including the ventricular myosin regulatory light-chain (RLC). The Myosin RLC mutation has been associated with a rare variant of cardiac hypertrophy defined by mid-left ventricular obstruction due to papillary muscle hypertrophy. This mutation was later found to cause ventricular and septal hypertrophy (3).
1. Poetter K, et al. Nat Genet 13(1):63-9, 1996
2. Macera MJ, et al. Genomics 13(3):829-31, 1992
3. Szczesna-Cordry D, et al. J Cell Sci 118(16):3675-83, 2005
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