84-5705-87　ARRB2 (Biotin) 100ug　555600

特徴

• 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.
• Applications:Suitable for use in ELISA.
• Other applications not tested.
• Recommended Dilution:Optimal dilutions to be determined by the researcher.
• Storage and Stability:Store product at 4°C if to be used immediately within two weeks.
• For long-term storage, aliquot to avoid repeated freezing and thawing and store at -20°C.
• Aliquots are stable at -20°C for 12 months after receipt.
• Dilute required amount only prior to immediate use.
• Further dilutions can be made in assay buffer.
• For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.