AKT1 anticorps (pThr308) (PE)

N° du produit ABIN1177033

Cet anticorps Souris Monoclonal détecte spécifiquement AKT1 dans ICS. Il présente une réactivité avec des échantillons de Humain et Souris. Il a été cité dans 5+ publications.

Aperçu rapide pour AKT1 anticorps (pThr308) (PE) (ABIN1177033)

Antigène: AKT1 (V-Akt Murine Thymoma Viral Oncogene Homolog 1 (AKT1))

Reactivité: Humain, Souris

Hôte: Souris

Clonalité: Monoclonal

Conjugué: Cet anticorp AKT1 est conjugé à/à la PE

Application: Intracellular Staining (ICS)

Clone: J1-223-371

Détail du produit anti-AKT1 anticorps (PE)

Épitope: pThr308

Marque: BD Phosflow™

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

Immunogène: Phosphorylated Human Akt1 Peptide

Isotype: IgG1 kappa

Information d'application

Indications d'application: This antibody detects Akt (pT308) in human and mouse cell lines. We have been unable to detect upregulated phosphorylation of Akt in activated leukocytes, such as whole blood and peripheral blood mononuclear cells.

Volume d'échantillon: 20 μL

Restrictions: For Research Use only

Stockage

Format: Liquid

Buffer: Aqueous buffered solution containing BSA 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: 4 °C

Stockage commentaire: Store undiluted at 4°C and protected from prolonged exposure to light. Do not freeze. The antibody was conjugated with R-PE under optimum conditions, and unconjugated antibody and free PE were removed.

Références pour anticorps anti-AKT1 (PE) (ABIN1177033)

De Falco, Avitabile, Totta, Straino, Spallotta, Cencioni, Torella, Rizzi, Porcelli, Zacheo, Di Vito, Pompilio, Napolitano, Melillo, Capogrossi, Pesce: "Altered SDF-1-mediated differentiation of bone marrow-derived endothelial progenitor cells in diabetes mellitus." dans: Journal of cellular and molecular medicine, Vol. 13, Issue 9B, pp. 3405-14, (2010) (PubMed).

Cantley, Neel: "New insights into tumor suppression: PTEN suppresses tumor formation by restraining the phosphoinositide 3-kinase/AKT pathway." dans: Proceedings of the National Academy of Sciences of the United States of America, Vol. 96, Issue 8, pp. 4240-5, (1999) (PubMed).

Ferrigno, Silver: "Regulated nuclear localization of stress-responsive factors: how the nuclear trafficking of protein kinases and transcription factors contributes to cell survival." dans: Oncogene, Vol. 18, Issue 45, pp. 6129-34, (1999) (PubMed).

Kandel, Hay: "The regulation and activities of the multifunctional serine/threonine kinase Akt/PKB." dans: Experimental cell research, Vol. 253, Issue 1, pp. 210-29, (1999) (PubMed).

Alessi, Andjelkovic, Caudwell, Cron, Morrice, Cohen, Hemmings: "Mechanism of activation of protein kinase B by insulin and IGF-1." dans: The EMBO journal, Vol. 15, Issue 23, pp. 6541-51, (1997) (PubMed).

Détails sur AKT1

Antigène: AKT1 (V-Akt Murine Thymoma Viral Oncogene Homolog 1 (AKT1))

Autre désignation: AKT

Sujet: Akt [also known as PKB (Protein kinase B) or RAC-PK (Related to the A and C kinases)] is a family of serine/threonine kinases that contains a pleckstrin homology (PH) domain. PH domains play important roles in signal transduction. There are three known isoforms of Akt in mammalian cells [Akt1 (alpha), Akt2 (beta) and Akt3 (gamma)], they are thought to be regulated similarly. Akt is activated by insulin and growth factors by a mechanism involving phosphoinositide 3-OH kinase. Phosphoinositide 3-OH kinase products bind to the PH domain, resulting in translocation of Akt to the plasma membrane and activation of Akt to phospho-Akt by upstream kinases. Akt is phosphorylated within the activation loop at threonine 308 (T308) and the C-terminus at serine 473. Phospho-Akt promotes cell survival by inhibiting apoptosis. Specifically, phospho-Akt1 has been shown to phosphorylate Bad, a member of the Bcl-2 family that promotes cell death. This phosphorylation results in the inactivation of the proapoptotic function of Bad. The Akt molecule is thus considered to link extracellular survival signals (growth factors) with the apoptotic machinery (Bad). Akt is also a key mediator of the metabolic effects of insulin. Additionally, Akt has been referred to as an oncogene because it has increased activity in a number of tumors. The J1-223.371 antibody recognizes Akt phosphorylated at T308.

Pathways: Signalisation PI3K-Akt, Signalisation RTK, TCR Signaling, AMPK Signaling, Interferon-gamma Pathway, Signalisation TLR, Fc-epsilon Receptor Signaling Pathway, EGFR Signaling Pathway, Neurotrophin Signaling Pathway, Response to Water Deprivation, Regulation of Actin Filament Polymerization, Carbohydrate Homeostasis, Glycosaminoglycan Metabolic Process, Cellular Glucan Metabolic Process, Regulation of Muscle Cell Differentiation, Cell-Cell Junction Organization, Regulation of Cell Size, Skeletal Muscle Fiber Development, Regulation of Carbohydrate Metabolic Process, Hepatitis C, Protein targeting to Nucleus, CXCR4-mediated Signaling Events, Signaling Events mediated by VEGFR1 and VEGFR2, Negative Regulation of intrinsic apoptotic Signaling, Thromboxane A2 Receptor Signaling, Signaling of Hepatocyte Growth Factor Receptor, Positive Regulation of fat Cell Differentiation, VEGFR1 Specific Signals, VEGF Signaling, L'effet Warburg