biological source
rabbit
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
Quality Level
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.
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.
Physical form
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
Other Notes
Synthetic peptide located within the following region: RLVIRKVQFAPEKPGPQPSAETTRHFLMSDRSLHLEASLDKELYYHGEPL
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
存储类别
10 - Combustible liquids
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
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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