Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human Arrestin 3 Antibodies:
anti-Rat (Rattus) Arrestin 3 Antibodies:
anti-Mouse (Murine) Arrestin 3 Antibodies:
Go to our pre-filtered search.
Human Polyclonal Arrestin 3 Primary Antibody for IHC, ELISA - ABIN185395
Lefkowitz, Shenoy: Transduction of receptor signals by beta-arrestins. in Science (New York, N.Y.) 2005
Show all 3 Pubmed References
Human Polyclonal Arrestin 3 Primary Antibody for 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. in Immunobiology 2011
Show all 2 Pubmed References
Cow (Bovine) Polyclonal Arrestin 3 Primary Antibody for IP, WB - ABIN152742
Chen, Rusnak, Lombroso, Sidhu: Dopamine promotes striatal neuronal apoptotic death via ERK signaling cascades. in The European journal of neuroscience 2009
Human Polyclonal Arrestin 3 Primary Antibody for ELISA, IHC - ABIN450082
Krishnamurthy, Galet, Ascoli: The association of arrestin-3 with the follitropin receptor depends on receptor activation and phosphorylation. in Molecular and cellular endocrinology 2003
Antihistamines displayed similar kinetic signatures on antagonizing histamine-induced beta-arrestin2 recruitment as compared to displacing radioligand binding from the H1R (show HRH1 Antibodies).
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 (show CXCL12 Antibodies) variant reproduced the G protein-dependent and beta-arrestin-dependent responses that are associated with normal CXCR4 (show CXCR4 Antibodies) signaling and lead to cell migration.
This work demonstrates that the expression of FSHR (show FSHR Antibodies) and LHCGR (show LHCGR Antibodies) can be induced in hGL5 cells but that the FSHR (show FSHR Antibodies)-dependent cAMP/PKA pathway is constitutively silenced, possibly to protect cells from FSHR (show FSHR Antibodies)-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 (show IGF1R Antibodies) to interact with each b-arrestin (show SAG Antibodies) isoform, depending on the presence of the ligand and demonstrates the antagonism between the two b-arrestin (show SAG Antibodies) isoforms in controlling IGF-1R (show IGF1R Antibodies) expression and function, which could be developed into a practical anti-IGF-1R (show IGF1R Antibodies) strategy for cancer therapy.
Results demonstrate that GPR3 (show GPR3 Antibodies) signals at the plasma membrane and can be silenced by GRK2 (show ADRBK1 Antibodies)/beta-arrestin overexpression. These results also strongly implicate the serine and/or threonine residues in the third intracellular loop in the regulation of GPR3 (show GPR3 Antibodies) activity.
EPCR (show PROCR Antibodies) occupancy recruits G-protein coupled receptor kinase 5 (show GRK5 Antibodies), thereby inducing beta-arrestin-2 biased PAR1 (show MARK2 Antibodies) signaling by both APC (show APC Antibodies) and thrombin (show F2 Antibodies). 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.
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 (show SAG Antibodies), -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 (show GRM5 Antibodies) offer significant advantages over first-generation inhibitors for the treatment of fragile X (show FMR1 Antibodies) and related disorders.
selective inactivation of the GPCR (show GPBAR1 Antibodies)-associated protein beta-arrestin 2 in hepatocytes of adult mice results in greatly increased hepatic GCGR (show GCGR Antibodies) signaling, leading to striking deficits in glucose homeostasis
AT1R (show AGTRAP Antibodies)-beta-arrestin-2 pathway signaling plays an important role in renal fibrosis.
These data suggest that one allele of arrestin-2 (show ARRB1 Antibodies) 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 (show OPRK1 Antibodies) 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 (show USP20 Antibodies) 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 (show AKT1 Antibodies)/GSK3 (show GSK3b Antibodies) signaling by D2 dopamine receptors.
Arrb2 physically interacts with the beta subunit (show POLG Antibodies) of trimeric G-proteins and Dishevelled (show DVL2 Antibodies), the interaction between arrb2 and Dishevelled (show DVL2 Antibodies) is promoted by the beta/gamma subunits of trimeric G-proteins.
results suggest that a functional interaction between beta-arrestin 2 and Smoothened (show SMO Antibodies) may be critical to regulate hedgehog (show SHH Antibodies) 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