M5187
Anti-Myosin VI (KA-15) antibody produced in rabbit
affinity isolated antibody, buffered aqueous solution
Synonym(s):
Anti-DFNA22, Anti-DFNB37
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About This Item
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biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen ~150 kDa
species reactivity
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
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... MYO6(4646)
General description
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.
Immunogen
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
Biochem/physiol Actions
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.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 1% BSA and 15 mM sodium azide.
Disclaimer
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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Storage Class Code
10 - Combustible liquids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Myosin VI: two distinct roles in endocytosis
Hasson T.
Journal of Cell Science, 116(17), 3453-3461 (2003)
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
Myosin VI is required for E-cadherin-mediated border cell migration
Geisbrecht E R, et al.
Nature Cell Biology, 4(8), 616-616 (2002)
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
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
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