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Merck
CN

M5187

Sigma-Aldrich

Anti-Myosin VI (KA-15) antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

别名:

Anti-DFNA22, Anti-DFNB37

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About This Item

MDL编号:
UNSPSC代码:
12352203
NACRES:
NA.41

生物来源

rabbit

质量水平

偶联物

unconjugated

抗体形式

affinity isolated antibody

抗体产品类型

primary antibodies

克隆

polyclonal

表单

buffered aqueous solution

分子量

antigen ~150 kDa

种属反应性

rat, canine

技术

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

运输

dry ice

储存温度

−20°C

靶向翻译后修饰

unmodified

基因信息

human ... MYO6(4646)

一般描述

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.

免疫原

synthetic peptide corresponding to an epitope within the C-terminal of human Myosin VI, with N-terminal cysteine added, conjugated to KLH.

应用

Anti-Myosin VI (KA-15) antibody has been used:
  • in immunoblotting
  • in immunocytochemistry
  • in immunofluorescence
  • immunohistochemistry
  • proximity ligation assay

生化/生理作用

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.

外形

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 1% BSA and 15 mM sodium azide.

免责声明

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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储存分类代码

10 - Combustible liquids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

常规特殊物品
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分析证书(COA)

Lot/Batch Number

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访问文档库

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
Myosin VI: two distinct roles in endocytosis
Hasson T.
Journal of Cell Science, 116(17), 3453-3461 (2003)
Shi-ming Yang et al.
Developmental dynamics : an official publication of the American Association of Anatomists, 238(8), 1897-1908 (2009-07-08)
Smad4 is the central intracellular mediator of transforming growth factor-beta (TGF-beta) signaling, which plays crucial roles in tissue regeneration, cell differentiation, embryonic development, and regulation of the immune system. Conventional Smad4 gene knockout results in embryonic lethality, precluding its use
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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