Invitrogen™ Phospho-ATM (Ser1981) Monoclonal Antibody (10H11.E12), eFluor™ 660, eBioscience™

Description

Description: This 10H11.E12 monoclonal antibody recognizes the human, mouse, and rat ataxia-telangiectasia (ATM) protein when phosphorylated on serine 1981. ATM belongs to the family of PI3 kinases and functions by coordinating cell cycle arrest and initiation of DNA repair through the phosphorylation of a multitude of substrates in response to DNA damage and oxidative stress. ATM exists as dimers or multimers in its inactive state but in response to DNA breaks, becomes activated through formation of monomers and autophosphorylation. Activated ATM is recruited to the site of DNA double strand breaks where it halts the cell cycle and initiates DNA repair through the phosphorylation of downstream DNA damage response pathway members. Loss of functional activity of ATM results in ataxia-telangiectasia (AT), a disease characterized by early onset neurodegeneration and predisposition to cancer. AT patients are immunodeficient, radiosensitive, and have an increased risk of certain cancer types such as lymphoma and leukemia. Applications Reported:This 10H11.E12 antibody has been reported for use in intracellular staining followed by flow cytometric analysis. Applications Tested: This 10H11.E12 antibody has been pre-titrated and tested by intracellular staining followed by flow cytometric analysis of normal human peripheral blood cells. This can be used at 5 μL (0.25 μg) per test. A test is defined as the amount (μg) of antibody that will stain a cell sample in a final vol...

Ataxia-telangiectasia Mutated (ATM) is a protein that belongs to the PI3/PI4 kinase family. Ataxia-telangiectasia is a rare autosomal recessive disorder characterized by progressive neurologic degeneration, immunologic deficiency, and an increased risk of lymphoid cancer. The ATM gene codes for a protein belonging to the phosphoinositide 3-kinase (PI3K) superfamily. ATM phosphorylates proteins instead of lipid and has many downstream targets that act as cell-cycle regulators including: P53, Mdm2, BRCA1, and SMC1. The ATM protein is responsible for repairing double-stranded DNA breaks that occur because of ionizing radiation and other mutagens. The ATM's C-terminal region has extensive homology to the catalytic domains of phosphatidylinositol 3-kinases (PI3 kinases). Studies have shown that ATM becomes autophosphorylated and upregulated by exposure to ionizing radiation. AT cells are hypersensitive to ionizing radiation, impaired in mediating the inhibition of DNA synthesis and display delays in p53 induction. Further, DNA damage caused by ionizing irradiation activates ATM-kinase, leading to a cascade of kinase reactions that regulate cell cycle, apoptosis, and DNA damage repair. Studies have linked ATM to apoptosis along with Nbs1 and Chk2 in the E2F1 pathway.