Foundational characteristics of cancer include proliferation, angiogenesis, migration, evasion of apoptosis, and cellular immortality. Find key markers for these cellular processes and antibodies to detect them.
The SUMOplot™ Analysis Program predicts and scores sumoylation sites in your protein. SUMOylation is a post-translational modification involved in various cellular processes, such as nuclear-cytosolic transport, transcriptional regulation, apoptosis, protein stability, response to stress, and progression through the cell cycle.
The Autophagy Receptor Motif Plotter predicts and scores autophagy receptor binding sites in your protein. Identifying proteins connected to this pathway is critical to understanding the role of autophagy in physiological as well as pathological processes such as development, differentiation, neurodegenerative diseases, stress, infection, and cancer.
> home > Products > Primary Antibodies > Antibody Collections > Anti-Wnt-Pathway (plus Lgr5) Antibodies > Anti-β-Arrestin 1 Antibody
Anti-β-Arrestin 1 Antibody
Mouse Monoclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB |
|---|---|
| Primary Accession | P49407 |
| Other Accession | NM_004041 |
| Reactivity | Human |
| Host | Mouse |
| Clonality | Monoclonal |
| Isotype | IgG2b |
| Immunogen | Recombinant human β-Arrestin 1 protein. |
| Purification | Affinity purified |
| Calculated MW | 51 KDa |
| Gene ID | 408 |
|---|---|
| Other Names | ARB1; ARR1; ARRB1; ARRB1_HUMAN; Arrestin 2; Arrestin beta 1; Arrestin beta-1; Beta-arrestin-1. |
| Dilution | WB~~1:500 |
| Format | Purified mouse monoclonal antibody in PBS(pH 7.4) containing with 0.09% (W/V) sodium azide and 50% glycerol. |
| Storage | Store at -20 °C.Stable for 12 months from date of receipt |
| Name | ARRB1 |
|---|---|
| Synonyms | ARR1 |
| 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 a 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 a 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. Required for atypical chemokine receptor ACKR2-induced RAC1-LIMK1-PAK1-dependent phosphorylation of cofilin (CFL1) and for the up-regulation 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. Negatively regulates the NOTCH signaling pathway by mediating the ubiquitination and degradation of NOTCH1 by ITCH. Participates in the recruitment of the ubiquitin- protein ligase to the receptor (PubMed:23886940). |
| Cellular Location | Cytoplasm. Nucleus. Cell membrane. Membrane, clathrin-coated pit. Cell projection, pseudopodium. 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). |
Research Areas
Citations (0)
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
Submit your citation using an Abcepta antibody to
info@abcepta.com, and receive a free "I Love Antibodies" mug.
info@abcepta.com, and receive a free "I Love Antibodies" mug.
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
Background
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 s
Abcepta welcomes feedback from its customers.
If you have used an Abcepta product and would like to share how it has performed, please click on the "Submit Review" button and provide the requested information. Our staff will examine and post your review and contact you if needed.
If you have any additional inquiries please email technical services at tech@abcepta.com.
$ 360.00
Cat# AP53399
Ordering Information
United States
AlbaniaAustraliaAustriaBelgiumBosnia & HerzegovinaBrazilBulgariaCanadaCentral AmericaChinaCroatiaCyprusCzech RepublicDenmarkEstoniaFinlandFranceGermanyGreeceHong KongHungaryIcelandIndiaIndonesiaIrelandIsraelItalyJapanLatviaLithuaniaLuxembourgMacedoniaMalaysiaMaltaNetherlandsNew ZealandNorwayPakistanPolandPortugalRomaniaSerbiaSingaporeSlovakiaSloveniaSouth AfricaSouth KoreaSpainSwedenSwitzerlandTaiwanTurkeyUnited KingdomUnited StatesVietnamWorldwideOthers
USA Headquarters
(888) 735-7227 / (858) 622-0099 or (858) 875-1900
Other Products
Shipping Information
Domestic orders (in stock items)
Shipped out the same day. Orders placed after 1 PM (PST) will ship out the next business day.
International orders
Contact your local distributors
