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Mouse Anti-MYO5A (AA 291-302) Recombinant Antibody (CBFYM-2990) (CBMAB-M3185-FY)

This product is mouse antibody that recognizes MYO5A. The antibody CBFYM-2990 can be used for immunoassay techniques such as: ELISA, WB.
See all MYO5A antibodies

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat
Clone
CBFYM-2990
Antibody Isotype
IgG1
Application
ELISA, WB

Basic Information

Immunogen
Synthetic peptide corresponding to residues 291-302 of human MYO6
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
Buffer
PBS, 1% BSA
Concentration
1 mg/mL
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
AA 291-302

Target

Full Name
MYOSIN VA
Introduction
This gene is one of three myosin V heavy-chain genes, belonging to the myosin gene superfamily. Myosin V is a class of actin-based motor proteins involved in cytoplasmic vesicle transport and anchorage, spindle-pole alignment and mRNA translocation. The protein encoded by this gene is abundant in melanocytes and nerve cells. Mutations in this gene cause Griscelli syndrome type-1, Griscelli syndrome type-3 and neuroectodermal melanolysosomal disease, or Elejalde disease. Multiple alternatively spliced transcript variants encoding different isoforms have been reported, but the full-length nature of some variants has not been determined.
Entrez Gene ID
Human4644
Mouse17918
Rat25017
UniProt ID
HumanQ9Y4I1
MouseQ99104
RatQ9QYF3
Alternative Names
Myosin VA; Myoxin; Dilute Myosin Heavy Chain, Non-Muscle; Myosin VA (Heavy Chain 12, Myoxin); Myosin, Heavy Polypeptide Kinase; Myosin Heavy Chain 12; Myosin-12; Myosin V
Function
Processive actin-based motor that can move in large steps approximating the 36-nm pseudo-repeat of the actin filament. Involved in melanosome transport. Also mediates the transport of vesicles to the plasma membrane. May also be required for some polarization process involved in dendrite formation.
Biological Process
Actin filament-based movement Source: UniProtKB
Actin filament organization Source: GO_Central
Cellular response to insulin stimulus Source: UniProtKB
Melanosome transport Source: UniProtKB
Post-Golgi vesicle-mediated transport Source: UniProtKB
Protein localization to plasma membrane Source: UniProtKB
Protein transport Source: UniProtKB-KW
Vesicle-mediated transport Source: UniProtKB
Vesicle transport along actin filament Source: UniProtKB
Cellular Location
Cytoskeleton
Actin cytoskeleton Source: GO_Central
Myosin complex Source: UniProtKB-KW
Cytosol
Cytosol Source: UniProtKB
Extracellular region or secreted
Extracellular exosome Source: UniProtKB
Other locations
Cytoplasm Source: UniProtKB
Filopodium tip Source: UniProtKB
Growth cone Source: UniProtKB
Insulin-responsive compartment Source: UniProtKB
Melanosome Source: UniProtKB
Membrane Source: UniProtKB
Neuron projection Source: UniProtKB
Ruffle
Involvement in disease
Griscelli syndrome 1 (GS1):
Rare autosomal recessive disorder that results in pigmentary dilution of the skin and hair, the presence of large clumps of pigment in hair shafts, silvery-gray hair and accumulation of melanosomes in melanocytes. GS1 patients show developmental delay, hypotonia and mental retardation, without apparent immune abnormalities.
Griscelli syndrome 3 (GS3):
Rare autosomal recessive disorder characterized by pigmentary dilution of the skin and hair, the presence of large clumps of pigment in hair shafts, and an accumulation of melanosomes in melanocytes, without other clinical manifestations.
Elejalde syndrome (ELEJAS):
Autosomal recessive condition characterized by skin hypopigmentation, the presence of large clumps of pigment in hair shafts, silvery-gray hair, accumulation of melanosomes in melanocytes and primary neurological abnormalities. Elejalde syndrome may be the same entity as Griscelli syndrome type I.

Xing, J., Gu, Y., Song, Y., Liu, Q., Chen, Q., Han, P., ... & Sui, F. (2023). MYO5A overexpression promotes invasion and correlates with low lymphocyte infiltration in head and neck squamous carcinoma. BMC cancer, 23(1), 1267.

Song, D., Ye, Z., Chen, F., Zhan, L., & Sun, X. (2023). circFNDC3B promotes esophageal squamous cell carcinoma progression by targeting MYO5A via miR-370-3p/miR-136-5p. BMC cancer, 23(1), 821.

Clark, H. E., Huang, Y. Y. M., Vance, G. H., & Alomari, A. K. (2022). Fatal melanoma with a novel MYO5A‐BRAF fusion and small associated conventional nevus: A case report and review of literature. Journal of Cutaneous Pathology, 49(9), 808-812.

Zhang, H., Wu, Z., Yang, L., Zhang, Z., Chen, H., & Ren, J. (2021). Novel mutations in the Myo5a gene cause a dilute coat color phenotype in mice. The FASEB Journal, 35(4), e21261.

Christen, M., de le Roi, M., Jagannathan, V., Becker, K., & Leeb, T. (2021). Myo5a frameshift variant in a miniature dachshund with coat color dilution and neurological defects resembling human griscelli syndrome type 1. Genes, 12(10), 1479.

Liang, X., Wu, Z., Shen, S., Niu, Y., Guo, Y., Liang, J., & Guo, W. (2020). LINC01980 facilitates esophageal squamous cell carcinoma progression via regulation of miR-190a-5p/MYO5A pathway. Archives of Biochemistry and Biophysics, 686, 108371.

Ito, J., Nakano, Y., Shima, H., Miwa, T., Kogure, Y., Isshiki, K., ... & Shimada, H. (2020). Central nervous system ganglioneuroblastoma harboring MYO5A-NTRK3 fusion. Brain tumor pathology, 37, 105-110.

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

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