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Mouse Anti-MYLK Recombinant Antibody (1D1) (CBMAB-A5734-LY)

The product is antibody recognizes MYLK. The antibody 1D1 immunoassay techniques such as: WB, ELISA.
See all MYLK antibodies
Published Data

Summary

Host Animal
Mouse
Specificity
Human
Clone
1D1
Antibody Isotype
IgG1, κ
Application
WB, ELISA

Basic Information

Immunogen
MYLK (NP_444253, 1710 a.a. ~ 1809 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.
Specificity
Human
Antibody Isotype
IgG1, κ
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
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
myosin light chain kinase
Introduction
This gene, a muscle member of the immunoglobulin gene superfamily, encodes myosin light chain kinase which is a calcium/calmodulin dependent enzyme. This kinase phosphorylates myosin regulatory light chains to facilitate myosin interaction with actin filaments to produce contractile activity. This gene encodes both smooth muscle and nonmuscle isoforms. In addition, using a separate promoter in an intron in the 3' region, it encodes telokin, a small protein identical in sequence to the C-terminus of myosin light chain kinase, that is independently expressed in smooth muscle and functions to stabilize unphosphorylated myosin filaments. A pseudogene is located on the p arm of chromosome 3. Four transcript variants that produce four isoforms of the calcium/calmodulin dependent enzyme have been identified as well as two transcripts that produce two isoforms of telokin. Additional variants have been identified but lack full length transcripts. [provided by RefSeq]
Entrez Gene ID
UniProt ID
Alternative Names
DKFZp686I10125; FLJ12216; KRP; MLCK; MLCK1; MLCK108; MLCK210; MSTP083; MYLK1; smMLCK
Function
Calcium/calmodulin-dependent myosin light chain kinase implicated in smooth muscle contraction via phosphorylation of myosin light chains (MLC). Also regulates actin-myosin interaction through a non-kinase activity. Phosphorylates PTK2B/PYK2 and myosin light-chains. Involved in the inflammatory response (e.g. apoptosis, vascular permeability, leukocyte diapedesis), cell motility and morphology, airway hyperreactivity and other activities relevant to asthma. Required for tonic airway smooth muscle contraction that is necessary for physiological and asthmatic airway resistance. Necessary for gastrointestinal motility. Implicated in the regulation of endothelial as well as vascular permeability, probably via the regulation of cytoskeletal rearrangements. In the nervous system it has been shown to control the growth initiation of astrocytic processes in culture and to participate in transmitter release at synapses formed between cultured sympathetic ganglion cells. Critical participant in signaling sequences that result in fibroblast apoptosis. Plays a role in the regulation of epithelial cell survival. Required for epithelial wound healing, especially during actomyosin ring contraction during purse-string wound closure. Mediates RhoA-dependent membrane blebbing. Triggers TRPC5 channel activity in a calcium-dependent signaling, by inducing its subcellular localization at the plasma membrane. Promotes cell migration (including tumor cells) and tumor metastasis. PTK2B/PYK2 activation by phosphorylation mediates ITGB2 activation and is thus essential to trigger neutrophil transmigration during acute lung injury (ALI). May regulate optic nerve head astrocyte migration. Probably involved in mitotic cytoskeletal regulation. Regulates tight junction probably by modulating ZO-1 exchange in the perijunctional actomyosin ring. Mediates burn-induced microvascular barrier injury; triggers endothelial contraction in the development of microvascular hyperpermeability by phosphorylating MLC. Essential for intestinal barrier dysfunction. Mediates Giardia spp.-mediated reduced epithelial barrier function during giardiasis intestinal infection via reorganization of cytoskeletal F-actin and tight junctional ZO-1. Necessary for hypotonicity-induced Ca2+ entry and subsequent activation of volume-sensitive organic osmolyte/anion channels (VSOAC) in cervical cancer cells. Responsible for high proliferative ability of breast cancer cells through anti-apoptosis.
Biological Process
Aorta smooth muscle tissue morphogenesis Source: BHF-UCL
Bleb assembly Source: UniProtKB
Cellular hypotonic response Source: UniProtKB
Positive regulation of calcium ion transport Source: UniProtKB
Positive regulation of cell migration Source: UniProtKB
Positive regulation of wound healing Source: UniProtKB
Protein phosphorylation Source: ProtInc
Smooth muscle contraction Source: UniProtKB
Tonic smooth muscle contraction Source: UniProtKB
Cellular Location
Cytoskeleton
stress fiber
Cytoplasm
Other locations
lamellipodium
Cleavage furrow
Note: Localized to stress fibers during interphase and to the cleavage furrow during mitosis.
Involvement in disease
Aortic aneurysm, familial thoracic 7 (AAT7):
A disease characterized by permanent dilation of the thoracic aorta usually due to degenerative changes in the aortic wall. It is primarily associated with a characteristic histologic appearance known as 'medial necrosis' or 'Erdheim cystic medial necrosis' in which there is degeneration and fragmentation of elastic fibers, loss of smooth muscle cells, and an accumulation of basophilic ground substance.
Megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS):
A form of megacystis-microcolon-intestinal hypoperistalsis syndrome, a congenital visceral myopathy primarily affecting females, and characterized by loss of smooth muscle contraction in the bladder and intestine. Affected individuals present at birth with functional obstruction of intestine, microcolon, dilation of bladder, and secondary hydronephrosis. The majority of cases have a fatal outcome due to malnutrition and sepsis, followed by multiorgan failure. MMIHS inheritance is autosomal recessive.
PTM
Can probably be down-regulated by phosphorylation. Tyrosine phosphorylation by ABL1 increases kinase activity, reverses MLCK-mediated inhibition of Arp2/3-mediated actin polymerization, and enhances CTTN-binding. Phosphorylation by SRC at Tyr-464 and Tyr-471 promotes CTTN binding.
The C-terminus is deglutamylated by AGTPBP1/CCP1, AGBL1/CCP4 and AGBL4/CCP6, leading to the formation of Myosin light chain kinase, smooth muscle, deglutamylated form. The consequences of C-terminal deglutamylation are unknown (By similarity).
Acetylated at Lys-608 by NAA10/ARD1 via a calcium-dependent signaling; this acetylation represses kinase activity and reduces tumor cell migration.

Hitsumoto, T., Tsukamoto, O., Matsuoka, K., Li, J., Liu, L., Kuramoto, Y., ... & Takashima, S. (2023). Restoration of Cardiac Myosin Light Chain Kinase Ameliorates Systolic Dysfunction by Reducing Superrelaxed Myosin. Circulation.

Kalra, J., Artamonov, M., Wang, H., Franke, A., Markowska, Z., Jin, L., ... & Somlyo, A. (2023). p90RSK2, a new MLCK mediates contractility in myosin light chain kinase null smooth muscle. Frontiers in Physiology, 14.

Sun, X., Sun, B. L., Sammani, S., Bermudez, T., Dudek, S. M., Camp, S. M., & Garcia, J. G. (2021). Genetic and epigenetic regulation of the non-muscle myosin light chain kinase isoform by lung inflammatory factors and mechanical stress. Clinical Science, 135(7), 963-977.

Oya, R., Tsukamoto, O., Sato, T., Kato, H., Matsuoka, K., Oshima, K., ... & Inohara, H. (2021). Phosphorylation of MYL12 by Myosin Light Chain Kinase Regulates Cellular Shape Changes in Cochlear Hair Cells. Journal of the Association for Research in Otolaryngology, 22, 425-441.

Srivastava, N., Tauseef, M., Amin, R., Joshi, B., Joshi, J. C., Kini, V., ... & Mehta, D. (2020). Noncanonical function of long myosin light chain kinase in increasing ER‐PM junctions and augmentation of SOCE. The FASEB Journal, 34(9), 12805.

Ding, J., Li, Z., Li, L., Ding, Y., Wang, D., Meng, S., ... & Wang, Y. (2020). Myosin light chain kinase inhibitor ML7 improves vascular endothelial dysfunction and permeability via the mitogen-activated protein kinase pathway in a rabbit model of atherosclerosis. Biomedicine & Pharmacotherapy, 128, 110258.

He, W. Q., Wang, J., Sheng, J. Y., Zha, J. M., Graham, W. V., & Turner, J. R. (2020). Contributions of myosin light chain kinase to regulation of epithelial paracellular permeability and mucosal homeostasis. International journal of molecular sciences, 21(3), 993.

Isobe, K., Raghuram, V., Krishnan, L., Chou, C. L., Yang, C. R., & Knepper, M. A. (2020). CRISPR-Cas9/phosphoproteomics identifies multiple noncanonical targets of myosin light chain kinase. American Journal of Physiology-Renal Physiology, 318(3), F600-F616.

Deng, J. T., Bhaidani, S., Sutherland, C., MacDonald, J. A., & Walsh, M. P. (2019). Rho-associated kinase and zipper-interacting protein kinase, but not myosin light chain kinase, are involved in the regulation of myosin phosphorylation in serum-stimulated human arterial smooth muscle cells. PLoS One, 14(12), e0226406.

Hodatsu, A., Fujino, N., Uyama, Y., Tsukamoto, O., Imai‐Okazaki, A., Yamazaki, S., ... & Yamagishi, M. (2019). Impact of cardiac myosin light chain kinase gene mutation on development of dilated cardiomyopathy. ESC Heart Failure, 6(2), 406-415.

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

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