Arrestin, beta 1 (ARRB1) (AA 262-409) antibody

Antigen: Arrestin, beta 1 (ARRB1)

Synonyms: ARB1, ARR1, BARRES, AW208571, MGC124269, MGC124270, 1200006I17Rik, G430100A01Rik, arrb1, MGC83787, arb1, arr1, barr1, MGC81940, betaarr1, ARRB1

Binding Site: AA 262-409

Clonality: Monoclonal (10)

Host: Mouse

Reactivity: Rat (Rattus)

Conjugate: Un-conjugated

Application: Western Blotting (WB)

Catalog no.: ABIN968033

Additional Information

Alternative name: beta-Arrestin1

Immunogen: Rat beta-Arrestin1

Cross-Reactivity: Mouse (Murine), Human

Format: Liquid

Isotype: IgG1

Clone: 10

Description: Beta-Arrestins were discovered due to their ability to modulate interactions between the phosphorylated beta2-Adrenergic receptors and G proteins. This modulation results in diminished beta2-Adrenergic receptor function, also known as desensitization. Because CoA and C27-bile acyl-CoAs to their (S)-stereoisomers, which are the only stereoisomers degraded by peroxisomal alpha-oxidation. Interestingly, AMACR mutations have been linked to some sensory motor neuropathies where accumulation of fatty acids and AMACR deficiencies correlate with pathogenesis. AMACR contains an N-terminal region required for mitochondrial localization, and a C-terminal peroxisomal targeting signal type 1 (PTS). AMACR mRNA is expressed preferarrestins are found at the synaptic terminals, they may provide a termination mechanism that allows the neurons to regain their original polarization and respond to a new neurotransmitter stimulus. The C-terminal region of arrestins is involved in selecting the phosphorylated and activated adrenergic receptors. The beta-Arrestin1 gene encodes a protein of 418 amino acids with an approximate molecular weight of 55kDa. beta-Arrestin1 protein is highly homologous to the 45kDa beta-Arrestin2. Both proteins are widely expressed, but are especially abundant in the central nervous system.
This antibody is routinely tested by western blot analysis of AMACR enzymatic activity found in the mitochondria relative to the peroxisomes differs depending on the species. Thus, AMACR is an enzyme critical for fatty acid degradation, and bile formation.

Characteristics: 1. Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2. Please refer to us for technical protocols.
3. Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
4. Source of all serum proteins is from USDA inspected abattoirs located in the United States.

Molecular Weight: 55 kDa

Comments:

Related Products: ABIN968555, ABIN967389

Application Details

Concentration: 250 µg/ml

Purity: Purified

Purification: Purified from tissue culture supernatant or ascites by affinity chromatography.

Buffer: Aqueous buffered solution containing BSA, glycerol.

Preservative: 0.09% Sodium azide.

Storage: Store undiluted at -20°C.

Restrictions: For Research Use only

Images

Western blot analysis of beta-Arrestin on a mouse macrophage lysate. Lane 1: 1:250, lane 2: 1:500, lane 3: 1:1000 dilution of the anti- beta-Arrestin antibody.

Publications

Product: Attramadal, Arriza, Aoki et al.: "Beta-arrestin2, a novel member of the arrestin/beta-arrestin gene family." in: The Journal of biological chemistry, Vol. 267, Issue 25, pp. 17882-90, 1992 (PubMed).

Gurevich, Dion, Onorato et al.: "Arrestin interactions with G protein-coupled receptors. Direct binding studies of wild type and mutant arrestins with rhodopsin, beta 2-adrenergic, and m2 muscarinic cholinergic receptors." in: The Journal of biological chemistry, Vol. 270, Issue 2, pp. 720-31, 1995 (PubMed).

DeFea, Zalevsky, Thoma et al.: "beta-arrestin-dependent endocytosis of proteinase-activated receptor 2 is required for intracellular targeting of activated ERK1/2." in: The Journal of cell biology, Vol. 148, Issue 6, pp. 1267-81, 2000 (PubMed).

Imamura, Huang, Dalle et al.: "beta -Arrestin-mediated recruitment of the Src family kinase Yes mediates endothelin-1-stimulated glucose transport." in: The Journal of biological chemistry, Vol. 276, Issue 47, pp. 43663-7, 2001 (PubMed).

Dalle, Imamura, Rose et al.: "Insulin induces heterologous desensitization of G-protein-coupled receptor and insulin-like growth factor I signaling by downregulating beta-arrestin-1." in: Molecular and cellular biology, Vol. 22, Issue 17, pp. 6272-85, 2002 (PubMed).