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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
CRIP1a (显示 CRIP1 ELISA试剂盒) can compete with beta-arrestins for interaction with C-terminal CB1R (显示 CNR1 ELISA试剂盒) domains that could affect agonist-driven, beta-arrestin-mediated internalization of the CB1R (显示 CNR1 ELISA试剂盒).
RACK1 (显示 GNB2L1 ELISA试剂盒) and beta-arrestin2 inhibit the dimerization of PDE4D5.
Suggest that fenoterol inhibited AICAR (显示 ATIC ELISA试剂盒)-induced AMPK (显示 PRKAA1 ELISA试剂盒) alpha1 activation and TNF-alpha (显示 TNF ELISA试剂盒) release through beta-arrestin-2 in THP-1 (显示 GLI2 ELISA试剂盒) cells.
Substance P (显示 TAC1 ELISA试剂盒) enhances tissue factor (显示 F3 ELISA试剂盒) release from granulocyte-macrophage colony-stimulating factor (显示 CSF2 ELISA试剂盒)-dependent macrophages via the p22phox (显示 CYBA ELISA试剂盒)/beta-arrestin 2/Rho A (显示 RHOA ELISA试剂盒) signaling pathway.
beta-arrestins regulate oxidative stress in a Nox4 (显示 NOX4 ELISA试剂盒)-dependent manner and increase fibrosis in heart failure.
Results demonstrate that betaArr2 signaling may be an important pathway for TAAR1 function and that the activation of the TAAR1-D2R complex negatively modulates GSK3b signaling
Role for engagement of BARR2 by the transactivated EGFR (显示 EGFR ELISA试剂盒) in agonist-specific regulation of delta receptor activation of ERK1/2 (显示 MAPK1/3 ELISA试剂盒)
Data suggest that thrombin (显示 F2 ELISA试剂盒) can directly activate PAR2 (显示 F2RL1 ELISA试剂盒) vasorelaxation, signal transduction (stimulating both calcium and MAP kinase (显示 MAPK1 ELISA试剂盒) responses), and triggering beta-arrestin recruitment (both beta-arrestin 1 (显示 ARRB1 ELISA试剂盒) and 2).
a beta-arrestin signalling cycle that is catalytically activated by the GPCR and energetically coupled to the endocytic machinery
The rare variants in ARRB2 were significantly associated with smoking status.
The fraction of arrestin2 molecules found in clusters larger than 100nm correlates with the magnitude of ligand-induced CCR5 (显示 CCR5 ELISA试剂盒) 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-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/GSK3 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.
These results reveal that the protective effect of deficiency of Arrb2 is due to loss of negative regulation of Akt (显示 AKT1 ELISA试剂盒).
that Insulin-like growth factor-1 (显示 IGF1 ELISA试剂盒) contributes to the mucosal repair by beta-arrestin2-mediated extracellular signal-regulated kinase signaling in experimental colitis
ARRB2 is not involved in hepatocellular carcinogenesis.
morphine activated JNK2 through an arrestin-independent Src- and PKC-dependent mechanism, whereas fentanyl activated JNK2 through a Src-GRK3/arrestin-2-dependent and PKC-independent mechanism.
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