Application
ARRB1 Antibody (C-term) western blot analysis in A549 cell line lysates (35ug/lane).This demonstrates the ARRB1 antibody detected the ARRB1 protein (arrow).Application
ARRB1 Antibody (C-term) immunohistochemistry analysis in formalin fixed and paraffin embedded human brain tissue followed by peroxidase conjugation of the secondary antibody and DAB staining.This data demonstrates the use of ARRB1 Antibody (C-term) for immunohistochemistry. Clinical relevance has not been evaluated.Application
Confocal immunofluorescent analysis of ARRB1 Antibody (C-term)(Cat#AP12005b) with A549 cell followed by Alexa Fluor 488-conjugated goat anti-rabbit lgG (green).Actin filaments have been labeled with Alexa Fluor 555 phalloidin (red). DAPI was used to stain the cell nuclear (blue).Application
ARRB1 Antibody (C-term) flow cytometric analysis of A549 cells (right histogram) compared to a negative control cell (left histogram).FITC-conjugated goat-anti-rabbit secondary antibodies were used for the analysis.| Product Name | ARRB1 Antibody (C-term) |
|---|---|
| Antibody Type | Primary Antibodies |
| Antigen Alias | ARRB1; ARR1; Beta-arrestin-1; Arrestin beta-1 |
| Clonality | Polyclonal |
|---|---|
| Isotype | Ig |
| Host Species | Rabbit |
| Tested Applications | WBIHCIFFC |
| WB:1:100~500 IHC |
|
| Species Reactivity | Human |
| Concentration | 1mg/ml |
| Gene Synonyms | ARR1 |
|---|---|
| Alternative Names | ARRB1 ARR1 Beta-arrestin-1 Arrestin beta-1 |
| Molecular Weight(MW) | 47066 Da |
| Function | 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. Involved in internalization of P2RY4 and UTP-stimulated 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 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). 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 resulting in ERK activation. 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). Inhibits ERK1/2 signaling in AGTR1- and AVPR2-mediated activation (reciprocal regulation). Is required for SP-stimulated endocytosis of NK1R and recruits c-Src/SRC to internalized NK1R resulting 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-stimulated AKT1 signaling. Is involved in IGF1-stimulated 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 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. May serve as nuclear messenger for GPCRs. Involved in OPRD1- stimulated transcriptional regulation by translocating to CDKN1B and FOS promoter regions and recruiting EP300 resulting in acetylation of histone H4. Involved in regulation of LEF1 transcriptional activity via interaction with DVL1 and/or DVL2 Also involved in regulation of receptors other than GPCRs 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 Binds phosphoinositides. Binds inositolhexakisphosphate (InsP6) (By similarity). Involved in IL8-mediated granule release in neutrophils |
| Tissue Specificity | This ARRB1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 343-371 amino acids from the C-terminal region of human ARRB1. |
| Cellular Localization | Cytoplasm. Nucleus. Cell membrane. Membrane, clathrin-coated pit (Probable). Cell projection, pseudopodium (By similarity). Cytoplasmic vesicle. Note=Translocates to the plasma membrane and colocalizes with antagonist-stimulated GPCRs. The monomeric form is predominantly located in the nucleus. The oligomeric form is located in the cytoplasm. Translocates to the nucleus upon stimulation of OPRD1 (By similarity) |
| Entrez Gene | 408 |
|---|---|
| Nucleotide Accession | NP_004032.2 |
Application
ARRB1 Antibody (C-term) western blot analysis in A549 cell line lysates (35ug/lane).This demonstrates the ARRB1 antibody detected the ARRB1 protein (arrow).
Application
ARRB1 Antibody (C-term) immunohistochemistry analysis in formalin fixed and paraffin embedded human brain tissue followed by peroxidase conjugation of the secondary antibody and DAB staining.This data demonstrates the use of ARRB1 Antibody (C-term) for immunohistochemistry. Clinical relevance has not been evaluated.
Application
Confocal immunofluorescent analysis of ARRB1 Antibody (C-term)(Cat#AP12005b) with A549 cell followed by Alexa Fluor 488-conjugated goat anti-rabbit lgG (green).Actin filaments have been labeled with Alexa Fluor 555 phalloidin (red). DAPI was used to stain the cell nuclear (blue).
Application
ARRB1 Antibody (C-term) flow cytometric analysis of A549 cells (right histogram) compared to a negative control cell (left histogram).FITC-conjugated goat-anti-rabbit secondary antibodies were used for the analysis.| Application Notes | WB:1:100~500 IHC |
|---|
| Form | Liquid |
|---|---|
| Storage Instructions | For short-term storage, store at 4° C. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles. |
| Storage Buffer | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
