Mouse Anti-ARRB2 Recombinant Antibody (3G1) (CBMAB-A3671-YC)

Mouse

Human

3G1

IgG2a

ELISA, ICC, IF, WB

ARRB2 (AAH07427.1, 300 a.a. ~ 409 a.a) partial recombinant protein with GST tag.

Human

IgG2a

Monoclonal

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Application	Note
IF(ICC)	10 µg/ml

Liquid

PBS, pH 7.4

None

Batch dependent

Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

arrestin, beta 2

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 si

Arrestin Beta 2; Non-Visual Arrestin-3; Arrestin 3; ARR2; ARB2; Arrestin, Beta 2; Beta-Arrestin-2; Arrestin Beta-2; BARR2;

Functions in regulating agonist-mediated G-protein coupled receptor (GPCR) signaling by mediating both receptor desensitization and resensitization processes. During homologous desensitization, beta-arrestins bind to the GPRK-phosphorylated receptor and sterically preclude its coupling to the cognate G-protein; the binding appears to require additional receptor determinants exposed only in the active receptor conformation. The beta-arrestins target many receptors for internalization by acting as endocytic adapters (CLASPs, clathrin-associated sorting proteins) and recruiting the GPRCs to the adapter protein 2 complex 2 (AP-2) in clathrin-coated pits (CCPs). However, the extent of beta-arrestin involvement appears to vary significantly depending on the receptor, agonist and cell type. Internalized arrestin-receptor complexes traffic to intracellular endosomes, where they remain uncoupled from G-proteins. Two different modes of arrestin-mediated internalization occur. Class A receptors, like ADRB2, OPRM1, ENDRA, D1AR and ADRA1B dissociate from beta-arrestin at or near the plasma membrane and undergo rapid recycling. Class B receptors, like AVPR2, AGTR1, NTSR1, TRHR and TACR1 internalize as a complex with arrestin and traffic with it to endosomal vesicles, presumably as desensitized receptors, for extended periods of time. Receptor resensitization then requires that receptor-bound arrestin is removed so that the receptor can be dephosphorylated and returned to the plasma membrane. Mediates endocytosis of CCR7 following ligation of CCL19 but not CCL21. Involved in internalization of P2RY1, P2RY4, P2RY6 and P2RY11 and ATP-stimulated internalization of P2RY2. Involved in phosphorylation-dependent internalization of OPRD1 and subsequent recycling or degradation. Involved in ubiquitination of IGF1R. Beta-arrestins function as multivalent adapter proteins that can switch the GPCR from a G-protein signaling mode that transmits short-lived signals from the plasma membrane via small molecule second messengers and ion channels to a beta-arrestin signaling mode that transmits a distinct set of signals that are initiated as the receptor internalizes and transits the intracellular compartment. Acts as signaling scaffold for MAPK pathways such as MAPK1/3 (ERK1/2) and MAPK10 (JNK3). ERK1/2 and JNK3 activated by the beta-arrestin scaffold are largely excluded from the nucleus and confined to cytoplasmic locations such as endocytic vesicles, also called beta-arrestin signalosomes. Acts as signaling scaffold for the AKT1 pathway. GPCRs for which the beta-arrestin-mediated signaling relies on both ARRB1 and ARRB2 (codependent regulation) include ADRB2, F2RL1 and PTH1R. For some GPCRs the beta-arrestin-mediated signaling relies on either ARRB1 or ARRB2 and is inhibited by the other respective beta-arrestin form (reciprocal regulation). Increases ERK1/2 signaling in AGTR1- and AVPR2-mediated activation (reciprocal regulation). Involved in CCR7-mediated ERK1/2 signaling involving ligand CCL19. Is involved in type-1A angiotensin II receptor/AGTR1-mediated ERK activity. Is involved in type-1A angiotensin II receptor/AGTR1-mediated MAPK10 activity. Is involved in dopamine-stimulated AKT1 activity in the striatum by disrupting the association of AKT1 with its negative regulator PP2A. Involved in AGTR1-mediated chemotaxis. Appears to function as signaling scaffold involved in regulation of MIP-1-beta-stimulated CCR5-dependent chemotaxis. Involved in attenuation of NF-kappa-B-dependent transcription in response to GPCR or cytokine stimulation by interacting with and stabilizing CHUK. Suppresses UV-induced NF-kappa-B-dependent activation by interacting with CHUK. The function is promoted by stimulation of ADRB2 and dephosphorylation of ARRB2. Involved in p53/TP53-mediated apoptosis by regulating MDM2 and reducing the MDM2-mediated degradation of p53/TP53. May serve as nuclear messenger for GPCRs. Upon stimulation of OR1D2, may be involved in regulation of gene expression during the early processes of fertilization. Also involved in regulation of receptors other than GPCRs. Involved in endocytosis of TGFBR2 and TGFBR3 and down-regulates TGF-beta signaling such as NF-kappa-B activation. Involved in endocytosis of low-density lipoprotein receptor/LDLR. Involved in endocytosis of smoothened homolog/Smo, which also requires GRK2. Involved in endocytosis of SLC9A5. Involved in endocytosis of ENG and subsequent TGF-beta-mediated ERK activation and migration of epithelial cells. Involved in Toll-like receptor and IL-1 receptor signaling through the interaction with TRAF6 which prevents TRAF6 autoubiquitination and oligomerization required for activation of NF-kappa-B and JUN. Involved in insulin resistance by acting as insulin-induced signaling scaffold for SRC, AKT1 and INSR. Involved in regulation of inhibitory signaling of natural killer cells by recruiting PTPN6 and PTPN11 to KIR2DL1. Involved in IL8-mediated granule release in neutrophils. Involved in the internalization of the atypical chemokine receptor ACKR3. Acts as an adapter protein coupling FFAR4 receptor to specific downstream signaling pathways, as well as mediating receptor endocytosis (PubMed:22282525, PubMed:23809162).

During the activation step of NLRP3 inflammasome, directly associates with NLRP3 leading to inhibition of proinflammatory cytokine release and inhibition of inflammation (PubMed:23809162).

Adult walking behavior Source: Ensembl
Brain development Source: Ensembl
Cell chemotaxis Source: UniProtKB
Desensitization of G protein-coupled receptor signaling pathway by arrestin Source: UniProtKB
Detection of temperature stimulus involved in sensory perception of pain Source: Ensembl
Dopamine receptor signaling pathway Source: ParkinsonsUK-UCL
Excitatory postsynaptic potential Source: ParkinsonsUK-UCL
Follicle-stimulating hormone signaling pathway Source: Ensembl
G protein-coupled receptor internalization Source: UniProtKB
G protein-coupled receptor signaling pathway Source: Reactome
Membrane organization Source: Reactome
Negative regulation of cysteine-type endopeptidase activity involved in apoptotic process Source: Ensembl
Negative regulation of GTPase activity Source: Ensembl
Negative regulation of interleukin-12 production Source: Ensembl
Negative regulation of interleukin-1 beta production Source: Ensembl
Negative regulation of interleukin-6 production Source: Ensembl
Negative regulation of natural killer cell mediated cytotoxicity Source: UniProtKB
Negative regulation of neuron apoptotic process Source: Ensembl
Negative regulation of NF-kappaB transcription factor activity Source: UniProtKB
Negative regulation of protein kinase B signaling Source: ParkinsonsUK-UCL
Negative regulation of protein phosphorylation Source: Ensembl
Negative regulation of protein ubiquitination Source: UniProtKB
Negative regulation of release of cytochrome c from mitochondria Source: Ensembl
Negative regulation of smooth muscle cell apoptotic process Source: Ensembl
Negative regulation of toll-like receptor signaling pathway Source: Ensembl
Negative regulation of tumor necrosis factor production Source: Ensembl
Platelet activation Source: Reactome
Positive regulation of calcium ion transport Source: Ensembl
Positive regulation of cardiac muscle cell differentiation Source: Ensembl
Positive regulation of collagen biosynthetic process Source: Ensembl
Positive regulation of DNA biosynthetic process Source: Ensembl
Positive regulation of epithelial cell apoptotic process Source: Ensembl
Positive regulation of ERK1 and ERK2 cascade Source: UniProtKB
Positive regulation of gene expression Source: Ensembl
Positive regulation of peptidyl-serine phosphorylation Source: Ensembl
Positive regulation of peptidyl-tyrosine phosphorylation Source: Ensembl
Positive regulation of protein kinase B signaling Source: Ensembl
Positive regulation of receptor internalization Source: UniProtKB
Positive regulation of synaptic transmission, dopaminergic Source: Ensembl
Proteasome-mediated ubiquitin-dependent protein catabolic process Source: UniProtKB
Protein deubiquitination Source: Reactome
Protein transport Source: UniProtKB-KW
Protein ubiquitination Source: UniProtKB
Receptor internalization Source: BHF-UCL
Transcription by RNA polymerase II Source: UniProtKB
Transforming growth factor beta receptor signaling pathway Source: BHF-UCL
Wnt signaling pathway, planar cell polarity pathway Source: Reactome

Cytoplasm; Nucleus; Cell membrane; Clathrin-coated pit; Cytoplasmic vesicle. Translocates to the plasma membrane and colocalizes with antagonist-stimulated GPCRs.

Phosphorylated at Thr-382 in the cytoplasm; probably dephosphorylated at the plasma membrane. The phosphorylation does not regulate internalization and recycling of ADRB2, interaction with clathrin or AP2B1.
The ubiquitination status appears to regulate the formation and trafficking of beta-arrestin-GPCR complexes and signaling. Ubiquitination appears to occur GPCR-specific. Ubiquitinated by MDM2; the ubiquitination is required for rapid internalization of ADRB2. Deubiquitinated by USP33; the deubiquitination leads to a dissociation of the beta-arrestin-GPCR complex. Stimulation of a class A GPCR, such as ADRB2, induces transient ubiquitination and subsequently promotes association with USP33. Stimulation of a class B GPCR promotes a sustained ubiquitination.
Hydroxylation by PHD2 modulates the rate of internalization by slowing down recruitment to the plasma membrane and inhibiting subsequent co-internalization with class A receptors.