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, immunoprecipitation, western blotting, immunocytochemistry, and immunohistochemical staining of formalin-fixed paraffin embedded tissue sections. (Fluorochrome conjugated 10H11.E12 is recommended for use in intracellular flow cytometry.).
Applications Tested: This 10H11.E12 antibody has been tested by immunohistochemistry of formalin-fixed paraffin embedded tissue using either high or low pH antigen retrieval and can be used at less than or equal to 10 µg/mL. This 10H11.E12 antibody has been tested by immunocytochemistry of methanol or formaldehyde-fixed and permeabilized cells and can be used at less than or equal to 10 µg/mL. It is recommended that the antibody be carefully titrated for optimal performance in the assay of interest.
Purity: Greater than 90%, as determined by SDS-PAGE.
Aggregation: Less than 10%, as determined by HPLC.
Filtration: 0.2 µm post-manufacturing filtered.
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.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Protein Aliases: A-T mutated; A-T mutated homolog; AT mutated; ATA; Ataxia telangiectasia gene mutated in human beings; Ataxia telangiectasia mutated; Ataxia telangiectasia mutated homolog; ATC; ATDC; ATE; DKFZp781A0353; MGC74674; Serine-protein kinase ATM; TEL1, telomere maintenance 1, homolog
Gene Aliases: AI256621; AT1; ATA; ATC; ATD; ATDC; ATE; ATM; C030026E19Rik; TEL1; TELO1