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Merck
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主要文件

AV48007

Sigma-Aldrich

Anti-ARRB2 antibody produced in rabbit

affinity isolated antibody

别名:

Anti-ARB2, Anti-ARR2, Anti-Arrestin, β 2, Anti-DKFZp686L0365

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About This Item

分類程式碼代碼:
12352203
NACRES:
NA.41

生物源

rabbit

品質等級

共軛

unconjugated

抗體表格

affinity isolated antibody

抗體產品種類

primary antibodies

無性繁殖

polyclonal

形狀

buffered aqueous solution

分子量

46 kDa

物種活性

human, bovine, dog, rabbit, rat, pig, horse

濃度

0.5 mg - 1 mg/mL

技術

immunohistochemistry: suitable
western blot: suitable

NCBI登錄號

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 ... ARRB2(409)

一般說明

Arrestin, β 2 (ARRB2), belongs to the arrestin family and suppresses cellular responses by desensitization of G-protein coupled receptor (GPCR). It also blocks β-adrenergic-mediated functions. Genetic variations in ARRB2 have been associated with Alzheimer′s disease and tardive dyskinesia.
Rabbit Anti-ARRB2 antibody recognizes pig, rabbit, canine, chicken, mouse, human, rat, bovine, and zebrafish ARRB2.

免疫原

Synthetic peptide directed towards the middle region of human ARRB2

應用

Rabbit Anti-ARRB2 antibody is suitable for western blot applications at a concentration of 1μg/ml. It can also be used for IHC applications at 4-8μg/ml.

生化/生理作用

Members of arrestin/beta-arrestin protein family are thought to participate in agonist-mediated desensitization of G-protein-coupled receptors and cause specific dampening of cellular responses to stimuli such as hormones, neurotransmitters, or sensory signals. ARRB2, like arrestin beta 1, was shown to inhibit beta-adrenergic receptor function in vitro. It is expressed at high levels in the central nervous system and may play a role in the regulation of synaptic receptors. Besides the brain, a cDNA for arrestin beta 2 was isolated from thyroid gland, and thus it may also be involved in hormone-specific desensitization of TSH receptors.Members of arrestin/beta-arrestin protein family are thought to participate in agonist-mediated desensitization of G-protein-coupled receptors and cause specific dampening of cellular responses to stimuli such as hormones, neurotransmitters, or sensory signals. Arrestin beta 2, like arrestin beta 1, was shown to inhibit beta-adrenergic receptor function in vitro. It is expressed at high levels in the central nervous system and may play a role in the regulation of synaptic receptors. Besides the brain, a cDNA for arrestin beta 2 was isolated from thyroid gland, and thus it may also be involved in hormone-specific desensitization of TSH receptors. Multiple alternatively spliced transcript variants have been found for this gene, but the full-length nature of some variants has not been defined.

序列

Synthetic peptide located within the following region: RLVIRKVQFAPEKPGPQPSAETTRHFLMSDRSLHLEASLDKELYYHGEPL

外觀

Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

免責聲明

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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儲存類別代碼

10 - Combustible liquids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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

Teng Jiang et al.
Current Alzheimer research, 11(4), 408-412 (2014-03-19)
Emerging evidence indicates that β-arrestin 2, an important regulator of G protein coupled receptors, is involved in the pathogenesis of Alzheimer's disease (AD). The aim of this study was to investigate the association between β-arrestin 2 gene (ARRB2) variation and
Y-J Liou et al.
European journal of neurology, 15(12), 1406-1408 (2008-12-04)
Tardive dyskinesia (TD) is a severe and potentially irreversible adverse effect of long-term antipsychotic treatment. Typical antipsychotics are commonly binding to the dopamine receptor D2 (DRD2), but the occurrence of antipsychotic-induced TD is rather delayed; therefore, the development of TD

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