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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
This work demonstrates that the expression of FSHR (Montrer FSHR Kits ELISA) and LHCGR (Montrer LHCGR Kits ELISA) can be induced in hGL5 cells but that the FSHR (Montrer FSHR Kits ELISA)-dependent cAMP/PKA pathway is constitutively silenced, possibly to protect cells from FSHR (Montrer FSHR Kits ELISA)-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 (Montrer IGF1R Kits ELISA) to interact with each b-arrestin (Montrer SAG Kits ELISA) isoform, depending on the presence of the ligand and demonstrates the antagonism between the two b-arrestin (Montrer SAG Kits ELISA) isoforms in controlling IGF-1R (Montrer IGF1R Kits ELISA) expression and function, which could be developed into a practical anti-IGF-1R (Montrer IGF1R Kits ELISA) strategy for cancer therapy.
Results demonstrate that GPR3 (Montrer GPR3 Kits ELISA) signals at the plasma membrane and can be silenced by GRK2 (Montrer ADRBK1 Kits ELISA)/beta-arrestin overexpression. These results also strongly implicate the serine and/or threonine residues in the third intracellular loop in the regulation of GPR3 (Montrer GPR3 Kits ELISA) activity.
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 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 fraction of arrestin2 molecules found in clusters larger than 100nm correlates with the magnitude of ligand-induced CCR5 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.
beta-arrestin2-biased negative modulators of mGlu5 (Montrer GRM5 Kits ELISA) offer significant advantages over first-generation inhibitors for the treatment of fragile X (Montrer FMR1 Kits ELISA) and related disorders.
selective inactivation of the GPCR (Montrer GPBAR1 Kits ELISA)-associated protein beta-arrestin 2 in hepatocytes of adult mice results in greatly increased hepatic GCGR (Montrer GCGR Kits ELISA) signaling, leading to striking deficits in glucose homeostasis
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.
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