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Primary Antibodies  >  Phospho Specific Antibodies

ATM pS1981 Antibody

Mouse Monoclonal 10H11.E12 IgG1 kappa
NCI Collaboration JCYIA Product
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100 µg
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ATM pS1981 Antibody Properties

Anti-ATM Protein Kinase pS1981 (MOUSE) Monoclonal Antibody - 200-301-400
Target Species
Known Cross Reactivity
human, mouse, rat
Monoclonal 10H11.E12 IgG1 kappa
ELISA : 1:20,000 - 1:100,000
IF Microscopy : 1:100 - 1:500
Western Blot : 1:200 - 1:2,000
Immunohistochemistry: Not Recommended
Other Dilution: User Optimized
Physical State
Liquid (sterile filtered)
Shipping Condition
Dry Ice
1.0 mg/mL by UV absorbance at 280 nm
0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2
0.01% (w/v) Sodium Azide
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ATM pS1981 Antibody Description

Anti ATM pS1981 Antibody is a phospho site specific antibody and recognizes the product of the ATM gene that is mutated in the hereditary disease ataxia-telangiectasia. ATM 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. Ideal for Cancer, Cell Signaling, Chromatin, Neuroscience and Signal Transduction research.
DKFZp781A0353 antibody, Human phosphatidylinositol 3 kinase homolog antibody, MGC74674 antibody, Serine protein kinase ATM antibody, T cell prolymphocytic leukemia antibody
Anti-ATM phospho S1981 Antibody was produced from a synthetic peptide S-L-A-F-E-E-G-Sp-Q-S-T-T-I-S-S corresponding to aa 1974-1988 of human ATM.
Immunogen Type
Post Translational Modification
Storage Condition
Store Anti-ATM phospho S1981 Antibody at -20° C prior to opening. Aliquot contents and freeze at -20° C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4° C as an undiluted liquid. Dilute only prior to immediate use.
Application Note
Protein A Purified Mab anti-ATM has been tested by ELISA and western blotting against both the native and recombinant forms of the protein. The antibody immunoprecipitates ATM from irradiated human and transfected mouse cells.  By immunofluoresence, foci are detected in irradiated human and mouse fibroblasts.  This antibody is not recommended for immunohistochemistry.  Instead, for IHC, use the clone 7C10D8 (p/n 200-301-500).
Anti-ATM phospho S1981 Monoclonal Antibody antibody is directed against human ATM and is useful in determining its presence in various assays. This monoclonal anti-ATM antibody recognizes the phosphorylated epitope in native and over-expressed 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.  Reactivity is observed against human ATM.  Cross reactivity with ATM from other mammalian sources has not been tested. The immunogen has 91% sequence homology with mouse ATM.
Disclaimer Note-General
This product is for research use only and is not intended for therapeutic or diagnostic applications. Please contact a technical service representative for more information. All products of animal origin manufactured by Rockland Immunochemicals are derived from starting materials of North American origin. Collection was performed in United States Department of Agriculture (USDA) inspected facilities and all materials have been inspected and certified to be free of disease and suitable for exportation. All properties listed are typical characteristics and are not specifications. All suggestions and data are offered in good faith but without guarantee as conditions and methods of use of our products are beyond our control. All claims must be made within 30 days following the date of delivery. The prospective user must determine the suitability of our materials before adopting them on a commercial scale. Suggested uses of our products are not recommendations to use our products in violation of any patent or as a license under any patent of Rockland Immunochemicals, Inc. If you require a commercial license to use this material and do not have one, then return this material, unopened to: Rockland Inc., P.O. BOX 5199, Limerick, Pennsylvania, USA.
General Reference
Specific Reference
Bakkenist, C. J. & Kastan, M. B. (2003). DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation. Nature 421, 499-506. 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. 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. 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. 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]. Pusapati, R. V., Rounbehler, R. J., Hong, S., Powers, J. T., Yan, M., Kiguchi, K., ... & Johnson, D. G. (2006). ATM promotes apoptosis and suppresses tumorigenesis in response to Myc. Proceedings of the National Academy of Sciences of the United States of America, 103(5), 1446-1451 Zhang, W., Peng, G., Lin, S. Y., & Zhang, P. (2011). DNA damage response is suppressed by the high cyclin-dependent kinase 1 activity in mitotic mammalian cells. Journal of Biological Chemistry, 286(41), 35899-35905.
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Primary Antibodies;
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Conjugation Reference
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