AKT1 antibody (pThr308) (PE)

Catalog No. ABIN1177033

This Mouse Monoclonal antibody specifically detects AKT1 in ICS. It exhibits reactivity toward Human and Mouse. It has been mentioned in 5+ publications

Quick Overview for AKT1 antibody (pThr308) (PE) (ABIN1177033)

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

Reactivity: Human, Mouse

Host: Mouse

Clonality: Monoclonal

Conjugate: This AKT1 antibody is conjugated to PE

Application: Intracellular Staining (ICS)

Clone: J1-223-371

Product Details anti-AKT1 Antibody (PE)

Binding Specificity: pThr308

Brand: BD Phosflow™

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

Immunogen: Phosphorylated Human Akt1 Peptide

Isotype: IgG1 kappa

Application Details

Application Notes: 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.

Sample Volume: 20 μL

Restrictions: For Research Use only

Handling

Format: Liquid

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

Preservative: Sodium azide

Precaution of Use: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Storage: 4 °C

Storage Comment: 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.

References for anti-AKT1 antibody (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." in: 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." in: 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." in: Oncogene, Vol. 18, Issue 45, pp. 6129-34, (1999) (PubMed).

Kandel, Hay: "The regulation and activities of the multifunctional serine/threonine kinase Akt/PKB." in: 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." in: The EMBO journal, Vol. 15, Issue 23, pp. 6541-51, (1997) (PubMed).

Target Details for AKT1

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

Alternative Name: AKT

Background: 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: PI3K-Akt Signaling, RTK Signaling, TCR Signaling, AMPK Signaling, Interferon-gamma Pathway, TLR Signaling, 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, Warburg Effect