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Rat (Rattus) Arrestin 3 Kit ELISA pour 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. dans Journal of psychopharmacology (Oxford, England) 2015
EPCR (Montrer PROCR Kits ELISA) occupancy recruits G-protein coupled receptor kinase 5 (Montrer GRK5 Kits ELISA), thereby inducing beta-arrestin-2 biased PAR1 (Montrer MARK2 Kits ELISA) signaling by both APC (Montrer APC Kits ELISA) and thrombin (Montrer F2 Kits ELISA). In
CCR5 (Montrer CCR5 PLURAL_@2305@) 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 (Montrer PAWR Kits ELISA) and P2Y12 (Montrer P2RY12 Kits ELISA) heterodimer internalization/endocytosis is required for beta-arrestin-2 recruitment to endosomes and up-regulation of Akt (Montrer AKT1 Kits ELISA) signaling; activation of PAR4 (Montrer PAWR Kits ELISA) but not of P2Y12 (Montrer P2RY12 Kits ELISA) drives internalization of the PAR4 (Montrer PAWR Kits ELISA)-P2Y12 (Montrer P2RY12 Kits ELISA) heterodimer. (PAR4 (Montrer PAWR Kits ELISA) = protease-activated receptor 4 (Montrer F2RL3 Kits ELISA); P2Y12 (Montrer P2RY12 Kits ELISA) = purinergic receptor P2Y (Montrer P2RY1 Kits ELISA), G-protein coupled, 12 protein; Akt (Montrer AKT1 Kits ELISA) = proto-oncogene (Montrer RAB1A Kits ELISA) protein c (Montrer PROC Kits ELISA)-akt (Montrer AKT1 Kits ELISA))
Analyzing the functional relevance of individual sites using phosphosite-deficient receptor mutants we found phosphorylation of the ADRB1 (Montrer ADRB1 Kits ELISA) 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 (Montrer OPRK1 Kits ELISA) 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 (Montrer DCLK3 Kits ELISA).
The downregulation of beta-arrestins 1/2 in saphenous vein endothelial cells (SVECs) prevented the shear stress-induced rise in levels of phosphorylation of Akt (Montrer AKT1 Kits ELISA) and endothelial nitric oxide synthase (eNOS (Montrer NOS3 Kits ELISA), Serine 1177).
CRIP1a (Montrer CRIP1 Kits ELISA) can compete with beta-arrestins for interaction with C-terminal CB1R (Montrer CNR1 Kits ELISA) domains that could affect agonist-driven, beta-arrestin-mediated internalization of the CB1R (Montrer CNR1 Kits ELISA).
RACK1 (Montrer GNB2L1 Kits ELISA) and beta-arrestin2 inhibit the dimerization of PDE4D5.
Suggest that fenoterol inhibited AICAR (Montrer ATIC Kits ELISA)-induced AMPK (Montrer PRKAA1 Kits ELISA) alpha1 activation and TNF-alpha (Montrer TNF Kits ELISA) release through beta-arrestin-2 in THP-1 (Montrer GLI2 Kits ELISA) cells.
The fraction of arrestin2 molecules found in clusters larger than 100nm correlates with the magnitude of ligand-induced CCR5 (Montrer CCR5 PLURAL_@2305@) internalization.
K2A mutations in arrestin-1 (Montrer SAG Kits ELISA), -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.
AT1R (Montrer AGTRAP Kits ELISA)-beta-arrestin-2 pathway signaling plays an important role in renal fibrosis.
These data suggest that one allele of arrestin-2 (Montrer ARRB1 Kits ELISA) 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 (Montrer OPRK1 Kits ELISA) 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 (Montrer USP20 Kits ELISA) 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 (Montrer AKT1 Kits ELISA)/GSK3 (Montrer GSK3b Kits ELISA) signaling by D2 dopamine receptors.
findings show for the first time that Ang II (Montrer AGT Kits ELISA) receptor signaling to beta-arrestin regulates ARF6 (Montrer ARF6 Kits ELISA) 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 (Montrer AKT1 Kits ELISA).
that Insulin-like growth factor-1 (Montrer IGF1 Kits ELISA) contributes to the mucosal repair by beta-arrestin2-mediated extracellular signal-regulated kinase signaling in experimental colitis
Arrb2 physically interacts with the beta subunit (Montrer POLG Kits ELISA) of trimeric G-proteins and Dishevelled (Montrer DVL2 Kits ELISA), the interaction between arrb2 and Dishevelled (Montrer DVL2 Kits ELISA) 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 (Montrer SHH Kits ELISA) 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