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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 IHC, ELISA - 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
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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
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.
Data indicate that a constitutively monomeric CXCL12 (显示 CXCL12 抗体) variant reproduced the G protein-dependent and beta-arrestin-dependent responses that are associated with normal CXCR4 (显示 CXCR4 抗体) signaling and lead to cell migration.
This work demonstrates that the expression of FSHR (显示 FSHR 抗体) and LHCGR (显示 LHCGR 抗体) can be induced in hGL5 cells but that the FSHR (显示 FSHR 抗体)-dependent cAMP/PKA pathway is constitutively silenced, possibly to protect cells from FSHR (显示 FSHR 抗体)-cAMP-PKA-induced apoptosis.
Lowering the level of cellular FLNA caused an elevation in RalA activity and resulted in selective interference with the normal intracellular trafficking and signaling of D3R through beta-arrestins.
This study reveals contrasting abilities of IGF-1R (显示 IGF1R 抗体) to interact with each b-arrestin (显示 SAG 抗体) isoform, depending on the presence of the ligand and demonstrates the antagonism between the two b-arrestin (显示 SAG 抗体) isoforms in controlling IGF-1R (显示 IGF1R 抗体) expression and function, which could be developed into a practical anti-IGF-1R (显示 IGF1R 抗体) strategy for cancer therapy.
Results demonstrate that GPR3 (显示 GPR3 抗体) signals at the plasma membrane and can be silenced by GRK2 (显示 ADRBK1 抗体)/beta-arrestin overexpression. These results also strongly implicate the serine and/or threonine residues in the third intracellular loop in the regulation of GPR3 (显示 GPR3 抗体) activity.
EPCR (显示 PROCR 抗体) occupancy recruits G-protein coupled receptor kinase 5 (显示 GRK5 抗体), thereby inducing beta-arrestin-2 biased PAR1 (显示 MARK2 抗体) signaling by both APC (显示 APC 抗体) and thrombin (显示 F2 抗体). In
CCR5 is highly expressed in active inflammatory bowel disease, and it has positive correlation with lymphocyte grade and negative correlation with expression of beta-arrestin2.
Data suggest that PAR4 (显示 PAWR 抗体) and P2Y12 (显示 P2RY12 抗体) heterodimer internalization/endocytosis is required for beta-arrestin-2 recruitment to endosomes and up-regulation of Akt (显示 AKT1 抗体) signaling; activation of PAR4 (显示 PAWR 抗体) but not of P2Y12 (显示 P2RY12 抗体) drives internalization of the PAR4 (显示 PAWR 抗体)-P2Y12 (显示 P2RY12 抗体) heterodimer. (PAR4 (显示 PAWR 抗体) = protease-activated receptor 4 (显示 F2RL3 抗体); P2Y12 (显示 P2RY12 抗体) = purinergic receptor P2Y (显示 P2RY1 抗体), G-protein coupled, 12 protein; Akt (显示 AKT1 抗体) = proto-oncogene (显示 RAB1A 抗体) protein c (显示 PROC 抗体)-akt (显示 AKT1 抗体))
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.
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.
beta-arrestin2-biased negative modulators of mGlu5 (显示 GRM5 抗体) offer significant advantages over first-generation inhibitors for the treatment of fragile X (显示 FMR1 抗体) and related disorders.
selective inactivation of the GPCR (显示 GPBAR1 抗体)-associated protein beta-arrestin 2 in hepatocytes of adult mice results in greatly increased hepatic GCGR (显示 GCGR 抗体) signaling, leading to striking deficits in glucose homeostasis
AT1R (显示 AGTRAP 抗体)-beta-arrestin-2 pathway signaling plays an important role in renal fibrosis.
These data suggest that one allele of arrestin-2 (显示 ARRB1 抗体) is unable to support normal locomotor behavior due to signaling and/or developmental defects.
Beta-arrestin-2 with beta-arrestin-1 shared common mechanisms to suppress podocyte autophagy by negative regulation of ATG12-ATG5 conjugation.
[beta]-arrestin2 regulates intestinal mucosal inflammation under both homeostatic and colitic conditions. Its mode of action involves negative regulation of T-cell activation and its requirement for induction of regulatory T cells.
Results suggest that the antipruritic effects of kappa opioid receptor (显示 OPRK1 抗体) agonists may not require betaarrestin2
that pro- and anti-inflammatory activities of beta-arrestin2 are determined by beta-arrestin2 ubiquitination and that changes in USP20 (显示 USP20 抗体) expression and/or activity can therefore regulate inflammatory responses
This shows that mood stabilizers lamotrigine, lithium and valproate can exert behavioral effects in mice by disrupting the beta-arrestin 2-mediated regulation of Akt (显示 AKT1 抗体)/GSK3 (显示 GSK3b 抗体) signaling by D2 dopamine receptors.
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