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Merck
CN

WH0009750M1

Sigma-Aldrich

Monoclonal Anti-C6orf32 antibody produced in mouse

clone 2E6-1B10, purified immunoglobulin, buffered aqueous solution

别名:

Anti-DIFF40, Anti-DIFF48, Anti-FAM65B, Anti-KIAA0386, Anti-PL48, Anti-chromosome 6 open reading frame 32

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关于此项目

UNSPSC代码:
12352203
NACRES:
NA.41
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生物来源

mouse

质量水平

偶联物

unconjugated

抗体形式

purified immunoglobulin

抗体产品类型

primary antibodies

克隆

2E6-1B10, monoclonal

表单

buffered aqueous solution

种属反应性

human

技术

indirect ELISA: suitable
western blot: 1-5 μg/mL

同位素/亚型

IgG2bκ

GenBank登记号

运输

dry ice

储存温度

−20°C

靶向翻译后修饰

unmodified

基因信息

human ... FAM65B(9750)

一般描述

FAM65B (family with sequence similarity 65, member B), also known as chromosome 6 open reading frame 32 (C6ORF32), is mapped to human chromosome 6p22.3. FAM65B is known to be expressed during embryonic and postnatal development stages in cochlea. The encoded protein is found to concentrate in the plasma membranes of the stereocilia of inner and outer hair cells of the inner ear.

免疫原

C6orf32 (AAH01232.1, 1 a.a. ~ 591 a.a) full-length recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.

Sequence
MLVGSQSFSPGGPNGIIRSQSFAGFSGLQERRSRCNSFIENSSALKKPQAKLKKMHNLGHKNNNPPKEPQPKRVEEVYRALKNGLDEYLEVHQTELDKLTAQLKDMKRNSRLGVLYDLDKQIKTIERYMRRLEFHISKVDELYEAYCIQRRLQDGASKMKQAFATSPASKAARESLTEINRSFKEYTENMCTIEVELENLLGEFSIKMKGLAGFARLCPGDQYEIFMKYGRQRWKLKGKIEVNGKQSWDGEETVFLPLIVGFISIKVTELKGLATHILVGSVTCETKELFAARPQVVAVDINDLGTIKLNLEITWYPFDVEDMTASSGAGNKAAALQRRMSMYSQGTPETPTFKDHSFFSNLPDDIFENGKAAEEKMPLSLSFSDLPNGDCALTSHSTGSPSNSTNPEITITPAEFNLSSLASQNEGMDDTSSASSRNSLGEGQEPKSHLKEEDPEEPRKPASAPSEACRRQSSGAGAEHLFLENDVAEALLQESEEASELKPVELDTSEGNITKQLVKRLTSAEVPMATDRLLSEGSVGGESEGCRSFLDGSLEDAFNGLLLALEPHKEQYKEFQDLNQEVMNLDDILKK

生化/生理作用

FAM65B (family with sequence similarity 65, member B) is recognized as a Ras homolog gene family, member A (RHOA) inhibitor and is involved in polarization. FAM65B regulates RhoA activity with the help of forkhead box O transcription factors. It binds to RhoA and blocks the GTP loading to RhoA. FAM65B deficiency in neutrophils leads to an increase in RhoA activity and causes defects in chemotaxis directionality and adhesion to endothelial cells under flow. It is involved in chemokine-stimulated migration and adhesion of Jurkat cells. Phosphorylation stabilizes FAM65B. FAM65B is a component of the inner ear and is involved in the process of hearing. Mutation in the gene is known to be associated with hearing loss in humans. FAM65B is associated with myotube formation and in the regulation of cell adhesion, polarization, and migration. Overexpression of the protein in myogenic and non-myogenic cells results in the formation of cellular protrusions. Hence, FAM65B might be involved in myoblast migration or cytoskeletal protein rearrangements that accompany myogenic differentiation.

外形

Solution in phosphate buffered saline, pH 7.4

法律信息

GenBank is a registered trademark of United States Department of Health and Human Services

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储存分类代码

10 - Combustible liquids

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)

法规信息

常规特殊物品
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历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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访问文档库

Fam65b is a new transcriptional target of FOXO1 that regulates RhoA signaling for T lymphocyte migration.
Rougerie P
Journal of Immunology (2013)
Fam65b is important for formation of the HDAC6-dysferlin protein complex during myogenic cell differentiation
Anuradha B
Faseb Journal (2014)
Front-signal-dependent accumulation of the RHOA inhibitor FAM65B at leading edges polarizes neutrophils
Kun Gao
Journal of Cell Science (2015)
Soonsang Yoon et al.
Developmental biology, 301(1), 70-81 (2006-12-08)
We have identified a gene by microarray analysis that is located on chromosome 6 (c6orf32), whose expression is increased during human fetal myoblast differentiation. The protein encoded by c6orf32 is expressed both in myogenic and non-myogenic primary cells isolated from
FAM65B is a membrane-associated protein of hair cell stereocilia required for hearing
Oscar Diaz-Horta
Proceedings of the National Academy of Sciences of the USA (2014)

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