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anti-Human Arrestin 3 Anticorps:
anti-Rat (Rattus) Arrestin 3 Anticorps:
anti-Mouse (Murine) Arrestin 3 Anticorps:
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Human Polyclonal Arrestin 3 Primary Antibody pour IHC, ELISA - ABIN185395
Lefkowitz, Shenoy: Transduction of receptor signals by beta-arrestins. dans Science (New York, N.Y.) 2005
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Human Polyclonal Arrestin 3 Primary Antibody pour 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. dans Immunobiology 2011
Show all 2 Pubmed References
Cow (Bovine) Polyclonal Arrestin 3 Primary Antibody pour IP, WB - ABIN152742
Chen, Rusnak, Lombroso, Sidhu: Dopamine promotes striatal neuronal apoptotic death via ERK signaling cascades. dans The European journal of neuroscience 2009
Human Polyclonal Arrestin 3 Primary Antibody pour ELISA, IHC - ABIN450082
Krishnamurthy, Galet, Ascoli: The association of arrestin-3 with the follitropin receptor depends on receptor activation and phosphorylation. dans 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 (Montrer CXCL12 Anticorps) variant reproduced the G protein-dependent and beta-arrestin-dependent responses that are associated with normal CXCR4 (Montrer CXCR4 Anticorps) signaling and lead to cell migration.
This work demonstrates that the expression of FSHR (Montrer FSHR Anticorps) and LHCGR (Montrer LHCGR Anticorps) can be induced in hGL5 cells but that the FSHR (Montrer FSHR Anticorps)-dependent cAMP/PKA pathway is constitutively silenced, possibly to protect cells from FSHR (Montrer FSHR Anticorps)-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 Anticorps) to interact with each b-arrestin (Montrer SAG Anticorps) isoform, depending on the presence of the ligand and demonstrates the antagonism between the two b-arrestin (Montrer SAG Anticorps) isoforms in controlling IGF-1R (Montrer IGF1R Anticorps) expression and function, which could be developed into a practical anti-IGF-1R (Montrer IGF1R Anticorps) strategy for cancer therapy.
Results demonstrate that GPR3 (Montrer GPR3 Anticorps) signals at the plasma membrane and can be silenced by GRK2 (Montrer ADRBK1 Anticorps)/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 Anticorps) activity.
EPCR (Montrer PROCR Anticorps) occupancy recruits G-protein coupled receptor kinase 5 (Montrer GRK5 Anticorps), thereby inducing beta-arrestin-2 biased PAR1 (Montrer MARK2 Anticorps) signaling by both APC (Montrer APC Anticorps) and thrombin (Montrer F2 Anticorps). 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 Anticorps) and P2Y12 (Montrer P2RY12 Anticorps) heterodimer internalization/endocytosis is required for beta-arrestin-2 recruitment to endosomes and up-regulation of Akt (Montrer AKT1 Anticorps) signaling; activation of PAR4 (Montrer PAWR Anticorps) but not of P2Y12 (Montrer P2RY12 Anticorps) drives internalization of the PAR4 (Montrer PAWR Anticorps)-P2Y12 (Montrer P2RY12 Anticorps) heterodimer. (PAR4 (Montrer PAWR Anticorps) = protease-activated receptor 4 (Montrer F2RL3 Anticorps); P2Y12 (Montrer P2RY12 Anticorps) = purinergic receptor P2Y (Montrer P2RY1 Anticorps), G-protein coupled, 12 protein; Akt (Montrer AKT1 Anticorps) = proto-oncogene (Montrer RAB1A Anticorps) protein c (Montrer PROC Anticorps)-akt (Montrer AKT1 Anticorps))
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 Anticorps), -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 (Montrer GRM5 Anticorps) offer significant advantages over first-generation inhibitors for the treatment of fragile X (Montrer FMR1 Anticorps) and related disorders.
selective inactivation of the GPCR (Montrer GPBAR1 Anticorps)-associated protein beta-arrestin 2 in hepatocytes of adult mice results in greatly increased hepatic GCGR (Montrer GCGR Anticorps) signaling, leading to striking deficits in glucose homeostasis
AT1R (Montrer AGTRAP Anticorps)-beta-arrestin-2 pathway signaling plays an important role in renal fibrosis.
These data suggest that one allele of arrestin-2 (Montrer ARRB1 Anticorps) 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 Anticorps) 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 Anticorps) 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 Anticorps)/GSK3 (Montrer GSK3b Anticorps) signaling by D2 dopamine receptors.
Arrb2 physically interacts with the beta subunit (Montrer POLG Anticorps) of trimeric G-proteins and Dishevelled (Montrer DVL2 Anticorps), the interaction between arrb2 and Dishevelled (Montrer DVL2 Anticorps) is promoted by the beta/gamma subunits of trimeric G-proteins.
results suggest that a functional interaction between beta-arrestin 2 and Smoothened (Montrer SMO Anticorps) may be critical to regulate hedgehog (Montrer SHH Anticorps) 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