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|+1 404 474 4654|
|+1 888 205 9894 (TF)|
Ataxia Telangiectasia Mutated (ATM) (pSer1981) antibody
|Synonyms||AT1, ATA, ATC, ATD, ATE, ATDC, TEL1, TELO1, MGC74674, DKFZp781A0353, AI256621, C030026E19Rik, ATM, Tefu, atm/tefu, dATM, tef, DmelCG6535, CG6535, Xatm|
Alternatives Immunohistochemistry (Frozen Sections) (IHC (fro)), Immunofluorescence (IF), Immunoprecipitation (IP), Western Blotting (WB)
|5 references available|
|Quantity||50 µg (1.0 mg/ml)|
|Price||Product not available in this region.|
|Gene ID||472, 11920|
|Immunogen||Corresponds to amino acids 1974-1988.|
|Cross-Reactivity||Human, Mouse (Murine)|
|Description||ATM, the gene mutated in the hereditary disease ataxia-telangiectasia, codes for aprotein kinase that acts as a master regulator of cellular responses to DNAdouble-strand breaks. ATM is normally inactive and the question of how it is activated inthe event of DNA damage (due to ionizing radiation for instance) is central tounderstanding its function. ATM protein is now shown to be present in undamaged cellsas an inactive dimer. Low doses of ionizing radiation, which induce only a few DNAbreaks, activate at least half of the total ATM protein present, possibly in response tochanges in chromatin structure. The ATM gene encodes a 370-kDa protein that belongsto the phosphoinositide 3-kinase (PI(3)K) superfamily, but which phosphorylatesproteins rather than lipids. The 350-amino-acid kinase domain at the carboxy terminusof this large protein is the only segment of ATM with an assigned function. Exposure ofcells to IR triggers ATM kinase activity, and this function is required for arrests in G1, Sand G2 phases of the cell cycle. Several substrates of the ATM kinase participate inthese IR-induced cell-cycle arrests. These include p53, Mdm2 and Chk2 in the G1checkpoint, Nbs1, Brca1, FancD2 and SMC1 in the transient IR-induced S-phase arrest,and Brca1 and hRad17 in the G2/M checkpoint. Alternate Names: 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-Ataxiatelangiectasia gene mutated antibody.|
|Specificity||This monoclonal anti-ATM antibody recognizes the phosphorylated epitope in native andoverexpressed proteins found in various tissues and extracts.Phosphorylated:Ser1981. Species Reactivity: Cross-reacts with Human and mouse.|
|Application Notes||Suggested working dilutions: immunohistochemistry 1/100-1/500,Western Blot|
|Buffer||0.02 M Potassium Phoshate, 0.15 M Sodium Chloride, pH 7.2. Preservative: 0.01% sodium azide.|
|Storage||Aliquot and store at -20C or -80C. Avoid freeze-thaw cycles.|
|Restrictions||For Research Use only|
|anti-Ataxia Telangiectasia Mutated (ATM) (pSer1981) antibody|
Bakkenist, Kastan: "DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation." in: Nature, Vol. 421, Issue 6922, pp. 499-506, 2003 (PubMed).
Kitagawa, Bakkenist, McKinnon et al.: "Phosphorylation of SMC1 is a critical downstream event in the ATM-NBS1-BRCA1 pathway." in: Genes & development, Vol. 18, Issue 12, pp. 1423-38, 2004 (PubMed).
Falck, Coates, Jackson: "Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage." in: Nature, Vol. 434, Issue 7033, pp. 605-11, 2005 (PubMed).
Bartkova, Horejsui, Koed et al.: "DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis." in: Nature, Vol. 434, Issue 7035, pp. 864-70, 2005 (PubMed).
Bartkova, Bakkenist, Rajpert-De Meyts et al.: "ATM activation in normal human tissues and testicular cancer." in: Cell cycle (Georgetown, Tex.), Vol. 4, Issue 6, pp. 838-45, 2005 (PubMed).