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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Arrestin, beta 2

beta-arrestin 2, arrestin-3
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. [provided by RefSeq, Mar 2012] (from NCBI)
Top mentioned proteins: IRBP, beta-arrestin, CAN, V1a, GPCR
Papers using beta-arrestin 2 antibodies
Leukotriene E4 activates peroxisome proliferator-activated receptor gamma and induces prostaglandin D2 generation by human mast cells.
Linden Rafael, In PLoS ONE, 2007
... Antibodies against arrestin-3 were purchased from Cell Signaling (Boston, MA) and Santa ...
Papers on beta-arrestin 2
G protein-coupled receptor kinase 6/β-arrestin 2 system in a rat model of dopamine supersensitivity psychosis.
Iyo et al., Mobara, Japan. In J Psychopharmacol, Dec 2015
G protein-coupled receptor kinase 6 (GRK6) and beta-arrestin 2 (ARRB2) play important roles in the trafficking of DRD2 by phosphorylation and internalization.
Beta-arrestin 2 dependence of delta opioid receptor agonists is correlated with alcohol intake.
van Rijn et al., West Lafayette, United States. In Br J Pharmacol, Nov 2015
We propose that variances in beta-arrestin2 recruitment contribute to the differential behavioral profile of DOR agonists.
Dopamine receptor D4 internalization requires a beta-arrestin and a visual arrestin.
Craft et al., Los Angeles, United States. In Cell Signal, Oct 2015
RESULTS: Immunohistochemistry studies of mouse retinas confirmed the expression of beta-arrestin 2, ARR1 and ARR4, as well as DRD4 in mouse cone photoreceptor inner segments.
Selective disruption of dopamine D2-receptors/beta-arrestin2 signaling by mood stabilizers.
Beaulieu et al., Québec, Canada. In J Recept Signal Transduct Res, Jun 2015
When administered chronically to mice lacking either D2 receptors or beta-arrestin 2, lamotrigine, lithium and valproate failed to affect Akt/GSK3 signaling as they do in normal littermates.
The effects of beta-arrestin1 deletion on acute cannabinoid activity, brain cannabinoid receptors and tolerance to cannabinoids in mice.
Vaghela et al., United States. In J Recept Signal Transduct Res, Feb 2015
CONTEXT: Previous studies have indicated a role for beta-arrestin2 in the regulation of brain cannabinoid effects and cannabinoid CB1 receptors, but whether beta-arrestin1 has a role has not been investigated.
β-Arrestins and G protein-coupled receptor trafficking.
Benovic et al., Philadelphia, United States. In Methods Enzymol, 2012
arrestin-2 and arrestin-3) are ubiquitously expressed and function to inhibit GPCR/G protein coupling and promote GPCR trafficking and arrestin-mediated signaling.
β-Arrestin2 mediates the initiation and progression of myeloid leukemia.
Reya et al., San Diego, United States. In Proc Natl Acad Sci U S A, 2012
the loss of beta-arrestin2 leads to a significant inhibition of beta-catenin stabilization, and ectopic activation of Wnt signaling
Arrestin scaffolds NHERF1 to the P2Y12 receptor to regulate receptor internalization.
Mundell et al., Bristol, United Kingdom. In J Biol Chem, 2012
Findings suggest a novel model by which arrestin can serve as an adaptor to promote NHERF1 interaction with a GPCR to facilitate effective NHERF1-dependent receptor internalization.
Evidence that behavioral phenotypes of morphine in β-arr2-/- mice are due to the unmasking of JNK signaling.
Walwyn et al., San Bernardino, United States. In Neuropsychopharmacology, 2012
removing beta-arrestin 2 reveals mu receptor activation of the JNK cascade in a ligand-specific manner explaining several behavioral phenotypes of beta-arr2-/- mice.
Inhibitor of G protein-coupled receptor kinase 2 normalizes vascular endothelial function in type 2 diabetic mice by improving β-arrestin 2 translocation and ameliorating Akt/eNOS signal dysfunction.
Kobayashi et al., Tokyo, Japan. In Endocrinology, 2012
G protein-coupled receptor kinase 2 inhibitor normalizes vascular endothelial function in type 2 diabetic mice by improving beta-arrestin 2 translocation and ameliorating Akt/eNOS signal dysfunction
Association study of the β-arrestin 2 gene (ARRB2) with opioid and cocaine dependence in a European-American population.
Berrettini et al., Philadelphia, United States. In Psychiatr Genet, 2012
Further studies are needed to determine whether variations in ARRB2 (or other MORIPs) are relevant to cocaine or opioid dependence in different ethnic populations or whether they confer a risk that is specific to dependence on other drugs of abuse
beta-Adrenoceptor inverse agonists in asthma.
Bond et al., Houston, United States. In Curr Opin Pharmacol, 2010
The data suggest that beta(2)-AR signaling is required to produce maximal airway inflammation and hyperresponsiveness, and the signaling pathway responsible for these effects is likely the non-canonical beta-arrestin-2 pathway.
Validating GSK3 as an in vivo target of lithium action.
Klein et al., Philadelphia, United States. In Biochem Soc Trans, 2009
However, lithium also inhibits inositol monophosphatase, several structurally related phosphomonoesterases, phosphoglucomutase and the scaffolding function of beta-arrestin-2.
Insulin action under arrestin.
James et al., Australia. In Cell Metab, 2009
In mouse models, beta-arrestin-2 controls whole-body insulin action by regulating assembly of a complex containing insulin receptor, c-Src, and Akt.
Physiologic and cardiac roles of beta-arrestins.
Rockman et al., Durham, United States. In J Mol Cell Cardiol, 2009
Beta-arrestin1 and beta-arrestin2 were initially identified by sequence homology to visual arrestins and by their ability to bind to and inactivate signaling of the beta-2-adrenergic receptor in a process known as desensitization.
Deficiency of a beta-arrestin-2 signal complex contributes to insulin resistance.
Pei et al., In Nature, 2009
in diabetic mouse models, beta-arrestin-2 is severely downregulated; knockdown of beta-arrestin-2 exacerbates insulin resistance, whereas administration of beta-arrestin-2 restores insulin sensitivity in mice
Akt/GSK3 signaling in the action of psychotropic drugs.
Caron et al., Québec, Canada. In Annu Rev Pharmacol Toxicol, 2008
Furthermore, investigations of the mechanism by which D2 dopamine receptors regulate Akt/GSK3 signaling strongly support the physiological relevance of a new modality of G protein-coupled receptor (GPCR) signaling involving the multifunctional scaffolding protein beta-arrestin 2. Elucidation of the contribution of multiple signaling pathways to the action of psychotropic drugs may provide a better biological understanding of psychiatric disorders and lead to more efficient therapeutics.
Looking at lithium: molecular moods and complex behaviour.
Caron et al., Québec, Canada. In Mol Interv, 2008
We also highlight recent findings suggesting that lithium could exert some of its behavioral effects by acting on a dopamine receptor regulated signaling complex composed of Akt, protein phosphatase 2A, and the multifunctional protein scaffold beta-arrestin 2.
An essential function for beta-arrestin 2 in the inhibitory signaling of natural killer cells.
Ge et al., Shanghai, China. In Nat Immunol, 2008
Here we show that the association of KIR2DL1, an inhibitory receptor of NK cells, with beta-arrestin 2 mediated recruitment of the tyrosine phosphatases SHP-1 and SHP-2 to KIR2DL1 and facilitated 'downstream' inhibitory signaling.
Beta-arrestin-mediated localization of smoothened to the primary cilium.
Lefkowitz et al., Durham, United States. In Science, 2008
findings indicate that, together, beta-arrestins and Kif3A may mediate the transport of Smo to the primary cilium
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