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HPA040824

Sigma-Aldrich

Anti-GRXCR1 antibody produced in rabbit

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

同義詞:

Anti-DFNB25, Anti-PPP1R88

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About This Item

分類程式碼代碼:
12352203
人類蛋白質圖譜編號:
NACRES:
NA.41

生物源

rabbit

共軛

unconjugated

抗體表格

affinity isolated antibody

抗體產品種類

primary antibodies

無性繁殖

polyclonal

產品線

Prestige Antibodies® Powered by Atlas Antibodies

形狀

buffered aqueous glycerol solution

物種活性

human

技術

immunohistochemistry: 1:50- 1:200

免疫原序列

GVKYKVSAGQALFNNLTKVLQQPSTDLEFDRVVIYTTCLRVVRTTFERCELVRKIFQNHRVKFEEKNIALNGEYGK

UniProt登錄號

運輸包裝

wet ice

儲存溫度

−20°C

目標翻譯後修改

unmodified

基因資訊

human ... GRXCR1(389207)

一般說明

Glutaredoxin and cysteine rich domain containing 1 (GRXCR1), also known as DFNB25, is encoded by the gene mapped to human locus 4p15.3-q12. The encoded protein is characterized with a cysteine-rich C-terminal region and a predicted GRX domain involved in reversible S-glutathionylation of proteins. GRXCR1 is a 290 residual protein, expressed mainly in fetal cochlea.

免疫原

glutaredoxin, cysteine rich 1 recombinant protein epitope signature tag (PrEST)

應用

All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project and as a result, are supported by the most extensive characterization in the industry.

The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.

生化/生理作用

Glutaredoxin and cysteine rich domain containing 1 (GRXCR1) plays an essential role in regulation of actin polymerization and organization in hair cells. Mutation in the gene is associated with the development of sensorineural autosomal-recessive nonsyndromic hearing impairment (arNSHI) and vestibular dysfunction.

特點和優勢

Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.

Every Prestige Antibody is tested in the following ways:
  • IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
  • Protein array of 364 human recombinant protein fragments.

聯結

Corresponding Antigen APREST79881

外觀

Solution in phosphate buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide.

法律資訊

Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany

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儲存類別代碼

10 - Combustible liquids

水污染物質分類(WGK)

WGK 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable


分析證明 (COA)

輸入產品批次/批號來搜索 分析證明 (COA)。在產品’s標籤上找到批次和批號,寫有 ‘Lot’或‘Batch’.。

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存取文件庫

Novel mutation in GRXCR1 at DFNB25 lead to progressive hearing loss and dizziness.
Mori K
The Annals of Otology, Rhinology, and Laryngology, 129S-134S (2015)
Homozygosity mapping reveals mutations of GRXCR1 as a cause of autosomal-recessive nonsyndromic hearing impairment.
Schraders M
American Journal of Human Genetics, 86(2), 138-147 (2010)
Characterization of two transgene insertional mutations at pirouette, a mouse deafness locus.
Odeh H
Audiology & Neuro-Otology, 9(5), 303-314 (2004)

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