beta Arrestin 1 anticorps (AA 262-409)

N° du produit ABIN968033

L’anticorps Souris Monoclonal anti-beta Arrestin 1 a été validé pour WB, IHC, IF et IP. Il convient pour détecter beta Arrestin 1 dans des échantillons de Humain, Souris et Rat. Il y a 5+ publications disponibles.

Aperçu rapide pour beta Arrestin 1 anticorps (AA 262-409) (ABIN968033)

Antigène: beta Arrestin 1 (ARRB1) (Arrestin, beta 1 (ARRB1))

Reactivité: Humain, Souris, Rat

Hôte: Souris

Clonalité: Monoclonal

Conjugué: Cet anticorp beta Arrestin 1 est non-conjugé

Application: Western Blotting (WB), Immunohistochemistry (IHC), Immunofluorescence (IF), Immunoprecipitation (IP)

Clone: 10-Beta

Détail du produit anti-beta Arrestin 1 anticorps

Épitope: AA 262-409

Réactivité croisée: Souris, Humain

Attributs du produit: 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.

Purification: The monoclonal antibody was purified from tissue culture supernatant or ascites by affinity chromatography.

Immunogène: Rat beta-Arrestin1 aa. 262-409

Isotype: IgG1

Information d'application

Commentaires:

Related Products: ABIN968555, ABIN967389

Restrictions: For Research Use only

Stockage

Format: Liquid

Concentration: 250 μg/mL

Buffer: Aqueous buffered solution containing BSA, glycerol, and ≤0.09 % sodium azide.

Agent conservateur: Sodium azide

Précaution d'utilisation: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Stock: -20 °C

Stockage commentaire: Store undiluted at -20° C.

Références pour anticorps anti-beta Arrestin 1 (ABIN968033)

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

Imamura, Huang, Dalle, Ugi, Usui, Luttrell, Miller, Lefkowitz, Olefsky: "beta -Arrestin-mediated recruitment of the Src family kinase Yes mediates endothelin-1-stimulated glucose transport." dans: The Journal of biological chemistry, Vol. 276, Issue 47, pp. 43663-7, (2001) (PubMed).

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

Gurevich, Dion, Onorato, Ptasienski, Kim, Sterne-Marr, Hosey, Benovic: "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." dans: The Journal of biological chemistry, Vol. 270, Issue 2, pp. 720-31, (1995) (PubMed).

Attramadal, Arriza, Aoki, Dawson, Codina, Kwatra, Snyder, Caron, Lefkowitz: "Beta-arrestin2, a novel member of the arrestin/beta-arrestin gene family." dans: The Journal of biological chemistry, Vol. 267, Issue 25, pp. 17882-90, (1992) (PubMed).

Détails sur beta Arrestin 1

Antigène: beta Arrestin 1 (ARRB1) (Arrestin, beta 1 (ARRB1))

Autre désignation: beta-Arrestin1

Sujet: 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.

Poids moléculaire: 55 kDa

Pathways: Positive Regulation of Peptide Hormone Secretion, Nuclear Hormone Receptor Binding, cAMP Metabolic Process, Myometrial Relaxation and Contraction, Synaptic Membrane, Regulation of G-Protein Coupled Receptor Protein Signaling, Phototransduction