M5187
Anti-Myosin VI (KA-15) antibody produced in rabbit
affinity isolated antibody, buffered aqueous solution
Synonyme(s) :
Anti-DFNA22, Anti-DFNB37
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About This Item
Produits recommandés
Source biologique
rabbit
Niveau de qualité
Conjugué
unconjugated
Forme d'anticorps
affinity isolated antibody
Type de produit anticorps
primary antibodies
Clone
polyclonal
Forme
buffered aqueous solution
Poids mol.
antigen ~150 kDa
Espèces réactives
rat, canine
Technique(s)
indirect immunofluorescence: 1:75 using cultured rat NRK cells
microarray: suitable
western blot: 1:1,000 using a whole extract of cultured dog MDCK cells
Conditions d'expédition
dry ice
Température de stockage
−20°C
Modification post-traductionnelle de la cible
unmodified
Informations sur le gène
human ... MYO6(4646)
Description générale
Myosin VI (MYO6) is localized to the Golgi complex and is expressed in the hair cells of the ear. It is a two-headed myosin with a short coiled-coil segment in its tail. The motor domain of MYO6 has two insertions. The gene encoding this protein is localized on chromosome 6q13.
Myosin VI is a relatively abundant widespread unconventional myosin composed of an N-terminal motor domain, a light chain binding neck region, a coiled-coiled region, and a highly conserved C-terminal domain. At the ′converter′ region, between the catalytic head and the neck region of Myosin VI, there is a characteristic linker about 50 amino acids long. Native Myosin VI is apparently a two-headed dimer of the heavy chains with each heavy chain bound to calmodulin light chain.
Immunogène
synthetic peptide corresponding to an epitope within the C-terminal of human Myosin VI, with N-terminal cysteine added, conjugated to KLH.
Application
Anti-Myosin VI (KA-15) antibody has been used:
- in immunoblotting
- in immunocytochemistry
- in immunofluorescence
- immunohistochemistry
- proximity ligation assay
Actions biochimiques/physiologiques
Myosin VI participates in the generation of cell shape change, cell motility, membrane remodeling, and possibly in organelle and particle transport or tethering. It is also involved in membrane trafficking pathways in cultured mammalian cells where it is associated with the membrane ruffles and the trans-Golgi network. The unusual direction of Myosin VI movement may suggest that it brings materials or membranes into the cell. Its activity in tissue cultured cells is thought to be regulated by phosphorylation. A mutation in Myosin VI was described recently in human autosomal dominant non syndromic hearing loss.
Forme physique
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 1% BSA and 15 mM sodium azide.
Clause de non-responsabilité
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Code de la classe de stockage
10 - Combustible liquids
Classe de danger pour l'eau (WGK)
WGK 3
Point d'éclair (°F)
Not applicable
Point d'éclair (°C)
Not applicable
Certificats d'analyse (COA)
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Myosin VI: two distinct roles in endocytosis
Hasson T.
Journal of Cell Science, 116(17), 3453-3461 (2003)
Myosin VI is required for E-cadherin-mediated border cell migration
Geisbrecht E R, et al.
Nature Cell Biology, 4(8), 616-616 (2002)
Kali Burke et al.
eNeuro, 9(3) (2022-05-26)
Aging leads to degeneration of the peripheral and central auditory systems, hearing loss, and difficulty understanding sounds in noise. Aging is also associated with changes in susceptibility to or recovery from damaging noise exposures, although the effects of the interaction
Maiko Miyagawa et al.
The Annals of otology, rhinology, and laryngology, 124 Suppl 1, 148S-157S (2015-05-23)
To elucidate the involvement of MYO6 mutations, known to be responsible for DFNA22/DFNB37, in Japanese hearing loss patients through the use of genetic analysis. Genomic variations responsible for hearing loss were identified by massively parallel DNA sequencing (MPS) of 63
Allison J Kalinousky et al.
Genes, 15(1) (2024-01-23)
Individuals with Kabuki syndrome type 1 (KS1) often have hearing loss recognized in middle childhood. Current clinical dogma suggests that this phenotype is caused by frequent infections due to the immune deficiency in KS1 and/or secondary to structural abnormalities of
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