Volume : 50 µg
Clone Number :
Aliases : ARB 2 antibody; ARB2 antibody; ARR 2 antibody; ARR2 antibody; ARRB 2 antibody; ARRB2 antibody; ARRB2_HUMAN antibody; Arrestin 3 antibody; Arrestin beta 2 antibody; Arrestin beta-2 antibody; BARR2 antibody; Beta-arrestin-2 antibody; DKFZp686L0365 antibody; HGNC : 712 antibody
Product Type : polyclonal Ab Antibody
Immunogen Species : Homo sapiens (Human)
UniProt ID : P32121
Immunogen : Recombinant Human Beta-arrestin-2 protein (222-369AA)
Raised in : Rabbit
Species Reactivity : Human
Tested Applications : ELISA
Background : Functions in reg µLating 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 intracell µLar 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-stim µLated internalization of P2RY2. Involved in phosphorylation-dependent internalization of OPRD1 and subsequent recycling or degradation. Involved in ubiquitination of IGF1R. Beta-arrestins function as m µLtivalent adapter proteins that can switch the GPCR from a G-protein signaling mode that transmits short-lived signals from the plasma membrane via small molec µLe 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 intracell µLar 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 reg µLation) 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 reg µLation). Increases ERK1/2 signaling in AGTR1- and AVPR2-mediated activation (reciprocal reg µLation). 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-stim µLated AKT1 activity in the striatum by disrupting the association of AKT1 with its negative reg µLator PP2A. Involved in AGTR1-mediated chemotaxis. Appears to function as signaling scaffold involved in reg µLation of MIP-1-beta-stim µLated CCR5-dependent chemotaxis. Involved in attenuation of NF-kappa-B-dependent transcription in response to GPCR or cytokine stim µLation by interacting with and stabilizing CHUK. Suppresses UV-induced NF-kappa-B-dependent activation by interacting with CHUK. The function is promoted by stim µLation of ADRB2 and dephosphorylation of ARRB2. Involved in p53/TP53-mediated apoptosis by reg µLating MDM2 and reducing the MDM2-mediated degradation of p53/TP53. May serve as nuclear messenger for GPCRs. Upon stim µLation of OR1D2, may be involved in reg µLation of gene expression during the early processes of fertilization. Also involved in reg µLation of receptors other than GPCRs. Involved in endocytosis of TGFBR2 and TGFBR3 and down-reg µLates 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 ADRBK1. 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 thro µgh the interaction with TRAF6 which prevents TRAF6 autoubiquitination and oligomerization required for activation of NF-kappa-B and JUN. Involved in ins µLin resistance by acting as ins µLin-induced signaling scaffold for SRC, AKT1 and INSR. Involved in reg µLation of inhibitory signaling of natural killer cells by recruiting PTPN6 and PTPN11 to KIR2DL1. Involved in IL8-mediated gran µLe release in neutrophils. Involved in the internalization of the atypical chemokine receptor ACKR3.
Clonality : polyclonal Ab
Isotype : IgG
Purification Method : >95%, Protein G purified
Conj µgate : HRP
Buffer : Preservative : 0.03% Proclin 300
Constituents : 50% Glycerol, 0.01M PBS, pH 7.4
Form : Liquid
Stroage : Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Target Names : ARRB2
Research Areas : Signal transduction