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ARRB1 Antibody HRP conjugated

http://www.mitotool.org/web/image/product.template/51452/image_1920?unique=2e10e05

Volume : 50 µg
Clone Number :
Aliases : ARB1 antibody; ARR1 antibody; ARRB1 antibody; ARRB1_HUMAN antibody; Arrestin 2 antibody; Arrestin beta 1 antibody; Arrestin beta-1 antibody; Beta-arrestin-1 antibody
Product Type : polyclonal Ab Antibody
Immunogen Species : Homo sapiens (Human)
UniProt ID : P49407
Immunogen : Recombinant Human Beta-arrestin-1 protein (1-260AA)
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. Involved in internalization of P2RY4 and UTP-stim µLated internalization of P2RY2. Involved in phosphorylation-dependent internalization of OPRD1 ands subsequent recycling. Involved in the degradation of cAMP by recruiting cAMP phosphodiesterases to ligand-activated receptors. 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). ERK1/2 activated by the beta-arrestin scaffold is largely excluded from the nucleus and confined to cytoplasmic locations such as endocytic vesicles, also called beta-arrestin signalosomes. Recruits c-Src/SRC to ADRB2 res µLting in ERK activation. 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). Inhibits ERK1/2 signaling in AGTR1- and AVPR2-mediated activation (reciprocal reg µLation). Is required for SP-stim µLated endocytosis of NK1R and recruits c-Src/SRC to internalized NK1R res µLting in ERK1/2 activation, which is required for the antiapoptotic effects of SP. Is involved in proteinase-activated F2RL1-mediated ERK activity. Acts as signaling scaffold for the AKT1 pathway. Is involved in alpha-thrombin-stim µLated AKT1 signaling. Is involved in IGF1-stim µLated AKT1 signaling leading to increased protection from apoptosis. Involved in activation of the p38 MAPK signaling pathway and in actin bundle formation. Involved in F2RL1-mediated cytoskeletal rearrangement and chemotaxis. Involved in AGTR1-mediated stress fiber formation by acting together with GNAQ to activate RHOA. 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. May serve as nuclear messenger for GPCRs. Involved in OPRD1-stim µLated transcriptional reg µLation by translocating to CDKN1B and FOS promoter regions and recruiting EP300 res µLting in acetylation of histone H4. Involved in reg µLation of LEF1 transcriptional activity via interaction with DVL1 and/or DVL2 Also involved in reg µLation of receptors other than GPCRs. 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. Binds phosphoinositides. Binds inositolhexakisphosphate (InsP6). Involved in IL8-mediated gran µLe release in neutrophils. Required for atypical chemokine receptor ACKR2-induced RAC1-LIMK1-PAK1-dependent phosphorylation of cofilin (CFL1) and for the up-reg µLation of ACKR2 from endosomal compartment to cell membrane, increasing its efficiency in chemokine uptake and degradation. 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 : ARRB1
Research Areas : Neuroscience; Signal transduction

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Conditions générales
Garantie satisfait ou remboursé de 30 jours
Expédition : 2-3 jours ouvrables