Anti-ARRB2 Antibody (C-Term)

Product Name

Anti-ARRB2 Antibody (C-Term)

View all beta-Arrestin 2 Antibodies

SKU/Catalog Number

M01443-1

Size

50 µl

Description

Boster Bio Anti-ARRB2 Antibody (C-Term) (Catalog # M01443-1). Tested in WB, IHC-P application(s). This antibody reacts with Human.

Storage & Handling

Maintain refrigerated at 2-8°C for up to 2 weeks. For long-term storage, store at -20°C in small aliquots to prevent freeze-thaw cycles.

Cite This Product

Anti-ARRB2 Antibody (C-Term) (Boster Biological Technology, Pleasanton CA, USA, Catalog # M01443-1)

Host

Rabbit

Contents

Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide.

Clonality

Polyclonal

Clone Number

1565CT164.36.80

Isotype

Rabbit IgG

Immunogen

This ARRB2 antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between 264-298 amino acids from human ARRB2.

*Blocking peptide can be purchased. Costs vary based on immunogen length. Contact us for pricing.

Reactive Species

M01443-1 is reactive to ARRB2 in Human

Applications

M01443-1 is guaranteed for IHC-P, WB Boster Guarantee

Observed Molecular Weight

Calculated molecular weight

46.106kDa

Background of beta-Arrestin 2

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 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 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.

Antibody Validation

Boster validates all antibodies on WB, IHC, ICC, Immunofluorescence, and ELISA with known positive control and negative samples to ensure specificity and high affinity, including thorough antibody incubations.

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Assay Dilutions Recommendation

The recommendations below provide a starting point for assay optimization. The actual working concentration varies and should be decided by the user.

WB: 1:2000
IHC-P: 1:25

Validation Images & Assay Conditions

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Anti-ARRB2 Antibody (C-Term) at 1:2000 dilution + human brain lysate
Lysates/proteins at 20 µg per lane.
Secondary
Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated at 1/10000 dilution.
Predicted band size : 46 kDa
Blocking/Dilution buffer: 5% NFDM/TBST.

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M01443-1 staining ARRB2 in human brain tissue sections by Immunohistochemistry (IHC-P -paraformaldehyde-fixed, paraffin-embedded sections). Tissue was fixed with formaldehyde and blocked with 3% BSA for 0. 5 hour at room temperature; antigen retrieval was by heat mediation with a citrate buffer (pH6). Samples were incubated with primary antibody (1/25) for 1 hours at 37°C. A undiluted biotinylated goat polyvalent antibody was used as the secondary antibody.

Gene/Protein Information For ARRB2 (Source: Uniprot.org, NCBI)

Alternative Names

ARB2; ARR2; ARRB2; arrestin 3; Arrestin beta-2; arrestin, beta 2; BARR2; betaArrestin 2; beta-Arrestin 2; beta-arrestin-2; DKFZp686L0365 ARRB2 ARB2, ARR2, BARR2 arrestin beta 2 beta-arrestin-2|arrestin 3|non-visual arrestin-3

For more info on ARRB2, check out the ARRB2 Infographic

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In this infographic, you will see the following information for ARRB2: database IDs, superfamily, protein function, synonyms, molecular weight, chromosomal locations, tissues of expression, subcellular locations, post-translational modifications, and related diseases, research areas & pathways. If you want to see more information included, or would like to contribute to it and be acknowledged, please contact [email protected].

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