| Field | Specification |
|---|---|
| Mfr No | |
| Alternative Names | Beta-arrestin-1;Arrestin beta-1;ARRB1;ARR1; |
| Cellular Localization | |
| Clonality | |
| Concentration | |
| Gene ID | |
| Host | |
| Immunogen | A synthetic peptide corresponding to a sequence at the N-terminus of human beta Arrestin 1, identical to the related rat and mouse sequences. |
| Isotype | |
| Molecular Weight | |
| Product Type | |
| Reactivity | |
| Reconstitution | |
| Target | |
| UniProt # |
Overview
Anti-beta Arrestin 1/ARRB1 Antibody Picoband® is an antibody targeting ARRB1. Common applications include WB, IHC, Flow Cytometry, ELISA. Key specifications include host: Rabbit; clonality: Polyclonal; isotype: Rabbit IgG; reactivity: Rat,Mouse,Human; observed MW: 18 kDa; calculated MW: 47066 MW.
Boster Bio Anti-beta Arrestin 1/ARRB1 Antibody catalog # PA2155. Tested in IHC, WB applications. This antibody reacts with Human, Mouse, Rat. The brand Picoband indicates this is a premium antibody that guarantees superior quality, high affinity, and strong signals with minimal background in Western blot applications. Only our best-performing antibodies are designated as Picoband, ensuring unmatched performance.
Key elements and design rationale
- Target: ARRB1 — Beta-arrestin-1
- Antibody format: Host: Rabbit; Clonality: Polyclonal; Isotype: Rabbit IgG
- Species reactivity: Rat,Mouse,Human
- Molecular weight guidance: Observed: 18 kDa; Calculated: 47066 MW
Specificity note: No cross reactivity with other proteins.
Biological background
Protein function (datasheet): 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. 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. .
Scientific background (datasheet): Arrestin, beta 1, also known as ARRB1, is a protein which in humans is encoded by the ARRB1 gene. Members of arrestin/beta-arrestin protein family are though to participate in agonist-mediated desensitization of G-protein-coupled receptors and cause specific dampening of cellular responses to stimuli such as hormones, neurotransmitters, or sensory signals. By fluorescence in situ hybridization, this gene is mapped to 11q13.4. Arrestin beta 1 is a cytosolic protein and acts as a cofactor in the beta-adrenergic receptor kinase (BARK) mediated desensitization of beta-adrenergic receptors. Besides the central nervous system, it is expressed at high levels in peripheral blood leukocytes, and thus the BARK/beta-arrestin system is believed to play a major role in regulating receptor-mediated immune functions.
Cellular localization (datasheet): Cytoplasm. Nucleus. Cell membrane. Membrane, clathrin-coated pit . Cell projection, pseudopodium . Cytoplasmic vesicle. 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). .
Sequence similarities (datasheet): Belongs to the arrestin family.
Research relevance and current trends
- Commonly studied in contexts related to G Protein Signaling,Heterotrimeric G Proteins,Neurodegenerative Disease,Neurology Process,Neuroscience,Neurotransmission,Receptors / Channels,Regulators,Signal Transduction,Signaling Pathway.
- Supports comparative expression analysis across conditions, genotypes, or treatments when paired with appropriate controls.
- Useful for confirming target presence and subcellular distribution using orthogonal readouts (e.g., microscopy vs. immunoblotting).
Common research applications
- Western blot (WB): Compare relative target abundance and apparent size/isoforms across samples; interpret bands in light of expected MW and potential PTMs.
- ELISA: Measure target abundance in compatible matrices using a standard-curve readout; ensure dilution linearity and appropriate controls.
- Immunohistochemistry (IHC): Assess tissue distribution and cell-type patterns; interpret staining with appropriate negative controls and antigen context.
- Flow cytometry: Quantify target-positive populations in single-cell suspensions; pair with viability and isotype/FMO controls conceptually.
Notes for experimental interpretation
- Consider isoforms, post-translational modifications, and processing that can shift apparent molecular weight or localization.
- Cross-reactivity (datasheet): No cross-reactivity with other proteins
- Use appropriate positive and negative controls (e.g., KO/KD, blocking peptide, or isotype controls) to support specificity interpretation.
As a polyclonal antibody, this reagent may recognize multiple epitopes on the target, which can improve detection robustness but may require careful specificity controls.
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