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AV48007

Sigma-Aldrich

Anti-ARRB2 antibody produced in rabbit

affinity isolated antibody

Synonym(s):

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

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

46 kDa

species reactivity

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

concentration

0.5 mg - 1 mg/mL

technique(s)

immunohistochemistry: suitable
western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... ARRB2(409)

General description

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.

Immunogen

Synthetic peptide directed towards the middle region of human ARRB2

Application

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.

Biochem/physiol Actions

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.

Sequence

Synthetic peptide located within the following region: RLVIRKVQFAPEKPGPQPSAETTRHFLMSDRSLHLEASLDKELYYHGEPL

Physical form

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

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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WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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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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