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抗Human Arrestin 3 抗体:
抗Rat (Rattus) Arrestin 3 抗体:
抗Mouse (Murine) Arrestin 3 抗体:
Human Polyclonal Arrestin 3 Primary Antibody for ELISA, WB - ABIN185395
Lefkowitz, Shenoy: Transduction of receptor signals by beta-arrestins. in Science (New York, N.Y.) 2005
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Human Polyclonal Arrestin 3 Primary Antibody for IHC (p), IP - ABIN250385
Zakrzewicz, Krasteva, Wilhelm, Dietrich, Wilker, Padberg, Wygrecka, Grau: Reduced expression of arrestin beta 2 by graft monocytes during acute rejection of rat kidneys. in Immunobiology 2011
Show all 2 Pubmed References
Cow (Bovine) Polyclonal Arrestin 3 Primary Antibody for IP, WB - ABIN152742
Chen, Rusnak, Lombroso, Sidhu: Dopamine promotes striatal neuronal apoptotic death via ERK signaling cascades. in The European journal of neuroscience 2009
Human Polyclonal Arrestin 3 Primary Antibody for ELISA, IHC - ABIN450082
Krishnamurthy, Galet, Ascoli: The association of arrestin-3 with the follitropin receptor depends on receptor activation and phosphorylation. in Molecular and cellular endocrinology 2003
These results show that b-arrestin1 (显示 SAG 抗体) and b-arrestin2 exert differential actions on PAC1R (显示 ADCYAP1R1 抗体) internalization and PAC1R (显示 ADCYAP1R1 抗体)-dependent ERK1/2 activation, and suggest that the two b-arrestin (显示 SAG 抗体) isoforms may be involved in fine and precise tuning of the PAC1R (显示 ADCYAP1R1 抗体) signaling pathways.
overexpression of beta-arrestin2 can inhibit the growth of renal cell carcinoma (显示 MOK 抗体) (RCC (显示 XRCC1 抗体)) cells in vitro, and beta-arrestin2 acts as a tumor suppressor gene in RCC (显示 XRCC1 抗体); the main mechanism may directly suppress the phosphorylation of IkBa (显示 NFKBIA 抗体) and indirectly suppress NFkB
Study investigated the association between five ARRB2 single nucleotide polymorphisms (SNPs): rs1045280, rs2036657, rs4790694, rs3786047 and rs452246, and response to antidepressant treatment in a sample of 569 patients with a major depressive episode treated for 6months: GG/GT patients for rs4522461 and AA/AC patients for rs4790694 had a lower response.
Itch/beta-arrestin2 complex binds SuFu and induces its Lys63-link (显示 SUFUH 抗体)ed polyubiquitylation without affecting its stability.
These data highlight a novel arrestin (显示 SAG 抗体)-mediated modulation of CREB (显示 CREB1 抗体) signalling, suggesting a reciprocal relationship between arrestin2 and arrestin3, wherein recruitment of arrestin3 restricts the ability of beta2AR (显示 ADRB2 抗体) to activate prolonged CREB (显示 CREB1 抗体) phosphorylation by precluding recruitment of an arrestin2/Src (显示 SRC 抗体)/p38 (显示 CRK 抗体) complex.
A novel regulatory role of GRK2 was proposed for the ubiquitination of beta-arrestin in the context of the PKC-mediated heterologous regulation of GPCRs.
USP33 (显示 USP33 抗体) may indirectly regulate the degradation and recycling of CXCR4 (显示 CXCR4 抗体) through deubiquitinating beta-arrestin2, promoting colorectal tumor cell metastasis.
Antihistamines displayed similar kinetic signatures on antagonizing histamine-induced beta-arrestin2 recruitment as compared to displacing radioligand binding from the H1R (显示 HRH1 抗体).
the internalization motif for the human neuropeptide Y4 receptor, which regulates arrestin-3 recruitment and receptor endocytosis, was identified.
Collectively, these data show that beta-arrestin2 phosphorylation at Thr(383) underlies beta-arrestin-dependent Erk1/2 activation by G protein-coupled receptors.
The fraction of arrestin2 molecules found in clusters larger than 100nm correlates with the magnitude of ligand-induced CCR5 internalization.
K2A mutations in arrestin-1 (显示 SAG 抗体), -2, and -3 significantly reduced their binding to active phosphorhodopsin.
Results reveal that multiple intramolecular interactions coordinately regulate arrestin2 interaction with clathrin, highlighting this interaction as a critical step in regulating receptor trafficking.
Spinal Arrb2 may serve as an intracellular gate for acute to chronic pain transition via desensitization of NMDAR (显示 GRIN1 抗体).
Knockout of mice beta-arrestin2, but not beta-arrestin1 (显示 ARRB1 抗体), results in deficits in plasticity mediated by mGlu1 (显示 GRM1 抗体) receptors in CA3 (显示 CA3 抗体) pyramidal neurons and by mGlu5 (显示 GRM5 抗体) receptors in CA1 (显示 CA1 抗体) pyramidal neurons.
beta-arrestin 2 can protect liver tissue from LPS (显示 TLR4 抗体)-induced injury via inhibition of TLR4 (显示 TLR4 抗体)/NF-kappaB (显示 NFKB1 抗体) signaling pathway-mediated inflammation.
Non-visual arrestins regulate the focal adhesion formation via small GTPases RhoA and Rac1 independently of G-protein-coupled receptors.
Arrb2 induces cardiomyocyte death by interacting with the p85 subunit of PI3K, and negatively regulating the formation of p85-PI3K/CaV3 survival complex, thus blocking activation of PI3K-Akt-GSK3beta cell survival signalling pathway in cardiac ischemia-reperfusion.
these results suggest that beta-arrestin2 down-regulation increases hepatocellular carcinoma cell migration and invasion ability
beta-Arrestin2 increases the Itch-mediated ubiquitylation of SuFu (显示 SUFUH 抗体)
Our data reveal beta-arrestin 1 (显示 ARRB1 抗体), beta-arrestin 2, and AT1R (显示 AGTRAP 抗体) as key regulatory molecules in the Frank-Starling mechanism, which involves length-dependent enhancement of cardiac myofilament Ca(2 (显示 CA2 抗体)+) sensitivity.
Arrestin (显示 SAG 抗体) beta2 deficiency-mediated intestinal progenitor/stem cell radioprotection relied on protracted NF-kappaB (显示 NFKB1 抗体) activation and subsequent suppression of PUMA (显示 BBC3 抗体) induction.
GIP stimulation induces a switch in GIPR recycling from a rapid endosomal to a slow trans-Golgi network (TGN) pathway. GPCR kinases and b-arrestin2 are required for this switch in recycling.
Arrb2 physically interacts with the beta subunit (显示 POLG 抗体) of trimeric G-proteins and Dishevelled (显示 DVL2 抗体), the interaction between arrb2 and Dishevelled (显示 DVL2 抗体) is promoted by the beta/gamma subunits of trimeric G-proteins.
results suggest that a functional interaction between beta-arrestin 2 and Smoothened (显示 SMO 抗体) may be critical to regulate hedgehog (显示 SHH 抗体) signaling in zebrafish development
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 encoding different isoforms have been found for this gene.
arrestin beta 2
, arrestin, beta 2
, arrestin 2
, beta-Arrestin 2
, arrestin beta-2
, arrestin 3
, beta arr2
, beta-arrestin 2