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Human Anti-MYL2 Recombinant Antibody (CBFYM-0008) (CBMAB-M0011-FY)

This product is human antibody that recognizes MYL2. The antibody CBFYM-0008 can be used for immunoassay techniques such as: FC.
See all MYL2 antibodies

Summary

Host Animal
Human
Specificity
Human, Mouse, Rat
Clone
CBFYM-0008
Antibody Isotype
IgG1
Application
FC

Basic Information

Specificity
Human, Mouse, Rat
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Preservative
0.05% Sodium azide
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Myosin Light Chain 2
Introduction
Thus gene encodes the regulatory light chain associated with cardiac myosin beta heavy chain. Ca+ triggers the phosphorylation of regulatory light chain that in turn triggers contraction. Mutations in this gene are associated with mid-left ventricular chamber type hypertrophic cardiomyopathy.
Entrez Gene ID
Human4633
Mouse17906
Rat363925
UniProt ID
HumanP10916
MouseP51667
RatP08733
Alternative Names
Myosin Light Chain 2; Myosin Light Chain 2, Slow Skeletal/Ventricular Muscle Isoform; Myosin, Light Polypeptide 2, Regulatory, Cardiac, Slow; Myosin, Light Chain 2, Regulatory, Cardiac, Slow; Cardiac Ventricular Myosin Light Chain 2; Ventricular Myosin Light Chain 2; Cardiac Myosin Light Chain 2; MLC-2s/V; MLC-2v
Function
Contractile protein that plays a role in heart development and function (PubMed:23365102, PubMed:32453731).

Following phosphorylation, plays a role in cross-bridge cycling kinetics and cardiac muscle contraction by increasing myosin lever arm stiffness and promoting myosin head diffusion; as a consequence of the increase in maximum contraction force and calcium sensitivity of contraction force. These events altogether slow down myosin kinetics and prolong duty cycle resulting in accumulated myosins being cooperatively recruited to actin binding sites to sustain thin filament activation as a means to fine-tune myofilament calcium sensitivity to force (By similarity).

During cardiogenesis plays an early role in cardiac contractility by promoting cardiac myofibril assembly (By similarity).
Biological Process
Cardiac muscle contraction Source: GO_Central
Cardiac myofibril assembly Source: BHF-UCL
Heart contraction Source: BHF-UCL
Heart development Source: UniProtKB
Muscle cell fate specification Source: GO_Central
Negative regulation of cell growth Source: BHF-UCL
Positive regulation of the force of heart contraction Source: UniProtKB
Regulation of striated muscle contraction Source: ProtInc
Regulation of the force of heart contraction Source: UniProtKB
Ventricular cardiac muscle tissue morphogenesis Source: BHF-UCL
Cellular Location
A band
Involvement in disease
Cardiomyopathy, familial hypertrophic 10 (CMH10):
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. Rarely, patients present a variant of familial hypertrophic cardiomyopathy, characterized by mid-left ventricular chamber thickening.
Myopathy, myofibrillar, 12, infantile-onset, with cardiomyopathy (MFM12):
A form of myofibrillar myopathy, a group of chronic neuromuscular disorders characterized at ultrastructural level by disintegration of the sarcomeric Z disk and myofibrils, and replacement of the normal myofibrillar markings by small dense granules, or larger hyaline masses, or amorphous material. MFM12 is an autosomal recessive, severe form characterized by progressive myopathy with onset shortly after birth, tremor or clonus at birth, and cardiomyopathy usually leading to death by 6 months of age. Skeletal and cardiac muscle tissues show fiber-type disproportion with small type I and normal sized type II fibers, and myofibrillar disorganization.
PTM
N-terminus is methylated by METTL11A/NTM1.
Phosphorylated by MYLK3 and MYLK2; promotes cardiac muscle contraction and function (By similarity). Dephosphorylated by PPP1CB complexed to PPP1R12B (By similarity). The phosphorylated form in adult is expressed as gradients across the heart from endocardium (low phosphorylation) to epicardium (high phosphorylation); regulates cardiac torsion and workload distribution (By similarity).

Yuan, C. C., Kazmierczak, K., Liang, J., Ma, W., Irving, T. C., & Szczesna-Cordary, D. (2022). Molecular basis of force-pCa relation in MYL2 cardiomyopathy mice: Role of the super-relaxed state of myosin. Proceedings of the National Academy of Sciences, 119(8), e2110328119.

Luo, X. L., Zhang, P., Liu, X., Huang, S., Rao, S. L., Ding, Q., & Yang, H. T. (2021). Myosin light chain 2 marks differentiating ventricular cardiomyocytes derived from human embryonic stem cells. Pflügers Archiv-European Journal of Physiology, 473(7), 991-1007.

Williams, J., Paudyal, A., Stewart, M., Cutillas, P., Cox, R. D., Tinker, A., & Metherell, L. (2021). A Shorter Myosin Light Chain Kinase 3 Isoform Maintains Myosin Light Chain 2 Phosphorylation but Does Not Attenuate the Dilated Cardiomyopathy Seen in C57BL/6N Mice. Circulation, 144(Suppl_1), A14037-A14037.

Sitbon, Y. H., Yadav, S., Kazmierczak, K., & Szczesna‐Cordary, D. (2020). Insights into myosin regulatory and essential light chains: a focus on their roles in cardiac and skeletal muscle function, development and disease. Journal of muscle research and cell motility, 41, 313-327.

Gil, W. S., Vidal, L. A. Á., Salguero, M. A. V., Cajiao, M. B., & Peña, C. V. (2020). Genetic variant affecting the myosin light chain 2 related to familial hypertrophic cardiomyopathy. Intractable & Rare Diseases Research, 9(4), 229-232.

Kazmierczak, K., Liang, J., Yuan, C. C., Yadav, S., Sitbon, Y. H., Walz, K., ... & Szczesna-Cordary, D. (2019). Slow-twitch skeletal muscle defects accompany cardiac dysfunction in transgenic mice with a mutation in the myosin regulatory light chain. The FASEB journal, 33(3), 3152.

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For research use only. Not intended for any clinical use.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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