| CatalogCode: | NB600-621 |
| ProductName: | ATM Antibody |
| Product Description: | Mouse Monoclonal anti-ATM (10H11.E12) [Ser1981] |
| Clone: | 10H11.E12 |
| Clonality: | Monoclonal |
| Immunogen: | Corresponds to amino acids 1974-1988. |
| Specificity: | This monoclonal anti-ATM antibody recognizes the phosphorylated epitope in native and overexpressed proteins found in various tissues and extracts. By ELISA reactivity against SLAFEEGSpQSTTISS at a 1:1600 dilution shows an absorbance >3.000; whereas reactivity against SLAFEEGSQSTTISS shows and absorbance of 0.145. |
| CrossReactivity: | Cross-reacts with Human and mouse. |
| Packaging: | 0.05 mg protein A purified Mouse ascites. |
| Control: | Native and recombinant forms of the protein. |
| Background: | ATM, the gene mutated in the hereditary disease ataxia-telangiectasia, codes for a protein kinase that acts as a master regulator of cellular responses to DNA double-strand breaks. ATM is normally inactive and the question of how it is activated in the event of DNA damage (due to ionizing radiation for instance) is central to understanding its function. ATM protein is now shown to be present in undamaged cells as an inactive dimer. Low doses of ionizing radiation, which induce only a few DNA breaks, activate at least half of the total ATM protein present, possibly in response to changes in chromatin structure. The ATM gene encodes a 370-kDa protein that belongs to the phosphoinositide 3-kinase (PI(3)K) superfamily, but which phosphorylates proteins rather than lipids. The 350-amino-acid kinase domain at the carboxy terminus of this large protein is the only segment of ATM with an assigned function. Exposure of cells to IR triggers ATM kinase activity, and this function is required for arrests in G1, S and G2 phases of the cell cycle. Several substrates of the ATM kinase participate in these IR-induced cell-cycle arrests. These include p53, Mdm2 and Chk2 in the G1 checkpoint; Nbs1, Brca1, FancD2 and SMC1 in the transient IR-induced S-phase arrest; and Brca1 and hRad17 in the G2/M checkpoint. See Bakkenist, C. J. & Kastan, M. B. Nature 421, 499-506 (2003) for a complete presentation of this antibody's specificity and utility. |
| ProductRef: | 1. Bakkenist, C. J. & Kastan, M. B. (2003). DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation. Nature 421, 499-506. 2. Kitagawa R, Bakkenist CJ, McKinnon PJ, Kastan MB. (2004) Phosphorylation of SMC1 is a critical downstream event in the ATM-NBS1-BRCA1 pathway. Genes Dev. 18(12):1423-38. 3. Falck, J. Coates, J. and Jackson, S.P. (2005) Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage. Nature 434: 605-611. 4. Bartkova J, Horejsi Z, Koed K, Kramer A, Tort F, Zieger K, Guldberg P, Sehested M, Nesland JM, Lukas C, Orntoft T, Lukas J, Bartek J. (2005) DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis. Nature 434; 864-870. 5. Bartkova J, Bakkenist CJ, Rajpert-De Meyts E, Skakkebaek NE, Sehested M, Lukas J, Kastan MB, Bartek J. (2005) ATM Activation in Normal Human Tissues and Testicular Cancer. Cell Cycle 4;(6) [Epub ahead of print]. |
| Storage: | Aliquot and store at -20C or -80C. Avoid freeze-thaw cycles. |
| Purity: | protein A purified |
| Host_Name: | Mouse |
| Buffer: | 0.02 M Potassium Phoshate, 0.15 M Sodium Chloride, pH 7.2 |
| ListPrice: | 295 |
| AppSummary: | ELISA, IF, WB |
| SpeciesSummary: | Hu, Mu |
| ALTnames: | anti-AT complementation group A antibody; anti-AT complementation group C antibody; anti-AT complementation group D antibody; anti-AT complementation group E antibody; anti-AT mutated protein antibody; anti-AT1 antibody; anti-ATA antibody; anti-Ataxia telangiectasia gene mutated antibody |
| ProteinTarget: | ATM |
| PackageSize: | 0.05 mg |
| Phosphorylated: | Ser1981 |
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