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Rat (Rattus) Arrestin 3 ELISA Kit for Sandwich ELISA - ABIN810989
Oda, Tadokoro, Takase, Kanahara, Watanabe, Shirayama, Hashimoto, Iyo: G protein-coupled receptor kinase 6/?-arrestin 2 system in a rat model of dopamine supersensitivity psychosis. in Journal of psychopharmacology (Oxford, England) 2015
This work demonstrates that the expression of FSHR (显示 FSHR ELISA试剂盒) and LHCGR (显示 LHCGR ELISA试剂盒) can be induced in hGL5 cells but that the FSHR (显示 FSHR ELISA试剂盒)-dependent cAMP/PKA pathway is constitutively silenced, possibly to protect cells from FSHR (显示 FSHR ELISA试剂盒)-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 ELISA试剂盒) to interact with each b-arrestin (显示 SAG ELISA试剂盒) isoform, depending on the presence of the ligand and demonstrates the antagonism between the two b-arrestin (显示 SAG ELISA试剂盒) isoforms in controlling IGF-1R (显示 IGF1R ELISA试剂盒) expression and function, which could be developed into a practical anti-IGF-1R (显示 IGF1R ELISA试剂盒) strategy for cancer therapy.
Results demonstrate that GPR3 (显示 GPR3 ELISA试剂盒) signals at the plasma membrane and can be silenced by GRK2 (显示 ADRBK1 ELISA试剂盒)/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 ELISA试剂盒) activity.
EPCR (显示 PROCR ELISA试剂盒) occupancy recruits G-protein coupled receptor kinase 5 (显示 GRK5 ELISA试剂盒), thereby inducing beta-arrestin-2 biased PAR1 (显示 MARK2 ELISA试剂盒) signaling by both APC (显示 APC ELISA试剂盒) and thrombin (显示 F2 ELISA试剂盒). 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 ELISA试剂盒) and P2Y12 (显示 P2RY12 ELISA试剂盒) heterodimer internalization/endocytosis is required for beta-arrestin-2 recruitment to endosomes and up-regulation of Akt (显示 AKT1 ELISA试剂盒) signaling; activation of PAR4 (显示 PAWR ELISA试剂盒) but not of P2Y12 (显示 P2RY12 ELISA试剂盒) drives internalization of the PAR4 (显示 PAWR ELISA试剂盒)-P2Y12 (显示 P2RY12 ELISA试剂盒) heterodimer. (PAR4 (显示 PAWR ELISA试剂盒) = protease-activated receptor 4 (显示 F2RL3 ELISA试剂盒); P2Y12 (显示 P2RY12 ELISA试剂盒) = purinergic receptor P2Y (显示 P2RY1 ELISA试剂盒), G-protein coupled, 12 protein; Akt (显示 AKT1 ELISA试剂盒) = proto-oncogene (显示 RAB1A ELISA试剂盒) protein c (显示 PROC ELISA试剂盒)-akt (显示 AKT1 ELISA试剂盒))
Analyzing the functional relevance of individual sites using phosphosite-deficient receptor mutants we found phosphorylation of the ADRB1 (显示 ADRB1 ELISA试剂盒) at Ser461/Ser462 in the distal part of the C-terminus to determine beta-arrestin2 recruitment and receptor internalization
Heterodimerization of the kappa opioid receptor (显示 OPRK1 ELISA试剂盒) and neurotensin receptor 1 contributes to a novel beta-arrestin-2-signaling pathway.
These results were consistent with those seen for beta2-AR. Thus, both beta-arrs negatively control AM1 receptor internalization, which depends on the C-tail of CLR (显示 DCLK3 ELISA试剂盒).
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 ELISA试剂盒), -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.
beta-arrestin2-biased negative modulators of mGlu5 (显示 GRM5 ELISA试剂盒) offer significant advantages over first-generation inhibitors for the treatment of fragile X (显示 FMR1 ELISA试剂盒) and related disorders.
selective inactivation of the GPCR (显示 GPBAR1 ELISA试剂盒)-associated protein beta-arrestin 2 in hepatocytes of adult mice results in greatly increased hepatic GCGR (显示 GCGR ELISA试剂盒) signaling, leading to striking deficits in glucose homeostasis
AT1R (显示 AGTRAP ELISA试剂盒)-beta-arrestin-2 pathway signaling plays an important role in renal fibrosis.
These data suggest that one allele of arrestin-2 (显示 ARRB1 ELISA试剂盒) 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 ELISA试剂盒) 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 ELISA试剂盒) 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 ELISA试剂盒)/GSK3 (显示 GSK3b ELISA试剂盒) signaling by D2 dopamine receptors.
findings show for the first time that Ang II (显示 AGT ELISA试剂盒) receptor signaling to beta-arrestin regulates ARF6 (显示 ARF6 ELISA试剂盒) activation. These proteins together control receptor endocytosis and ultimately cell migration.
Arrb2 physically interacts with the beta subunit (显示 POLG ELISA试剂盒) of trimeric G-proteins and Dishevelled (显示 DVL2 ELISA试剂盒), the interaction between arrb2 and Dishevelled (显示 DVL2 ELISA试剂盒) is promoted by the beta/gamma subunits of trimeric G-proteins.
results suggest that a functional interaction between beta-arrestin 2 and Smoothened may be critical to regulate hedgehog (显示 SHH ELISA试剂盒) 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