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ATM antibody (Ataxia Telangiectasia Mutated) (AA 1974-1988)

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AA 1974-1988
(76), (22), (17), (16), (13), (13), (8), (8), (7), (6), (6), (5), (4), (4), (4), (4), (3), (3), (3), (3), (2), (2), (2), (2), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1)
(303), (75), (30), (6), (4), (1), (1)
(218), (58), (16), (9), (4)
Clonality (Clone)
Monoclonal ()
This ATM antibody is un-conjugated
(8), (8), (6), (6), (6), (6), (4), (2), (2), (2), (2), (2), (2), (2), (2), (1)
Western Blotting (WB), ELISA, Immunohistochemistry (IHC), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))
(175), (79), (71), (52), (44), (43), (25), (22), (16), (11), (7), (5), (4), (2), (2), (1), (1), (1), (1)
Pubmed 5 references available
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Quantity 0.05 mg
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Immunogen Corresponds to amino acids 1974-1988.
Clone 7C10D8
Isotype IgG2a
Specificity This monoclonal anti-ATM recognizes the phosphorylated epitope in native and overexpressed proteins found in various tissues and extracts.
Purification Protein A purified
Alternative Name ATM (ATM Antibody Abstract)
Background 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.
Gene Symbol: ATM
Gene ID 472, 11920
Pathways p53 Signaling, Apoptosis, DNA Damage Repair
Application Notes This antibody clone has been optimized for IHC, but may also be used for western blotting, immunoprecipitation or immunofluorescence microscopy. Indirect immunoperoxidase staining on formaldehyde-fixed, de-paraffinized tissue sections and/or formalin-fixed cultured cells are recommended when using this antibody as described in Bartkova et al 2005. NB 600-621 produced from clone 10H11.E12 has been optimized for WB, IP and IF.
Recommended dilutions: ELISA 1:10000 - 1:50000, Immunohistochemistry 1:100 - 1:500, Immunohistochemistry-Paraffin, Western Blot 1:500- 1:2000
Restrictions For Research Use only
Buffer 0.02 M Potassium pH oshate, 0.15 M Sodium Chloride, pH 7.2, Sodium Azide
Preservative Sodium azide
Precaution of Use WARNING: Reagents contain sodium azide. Sodium azide is very toxic if ingested or inhaled. Avoid contact with skin, eyes, or clothing. Wear eye or face protection when handling. If skin or eye contact occurs, wash with copious amounts of water. If ingested or inhaled, contact a physician immediately. Sodium azide yields toxic hydrazoic acid under acidic conditions. Dilute azide-containing compounds in running water before discarding to avoid accumulation of potentially explosive deposits in lead or copper plumbing.
Handling Advice Avoid freeze-thaw cycles
Storage -20 °C
Storage Comment Aliquot and store at -20 °C or -80 °C.
Supplier Images
Immunohistochemistry (IHC) image for anti-ATM antibody (Ataxia Telangiectasia Mutated) (AA 1974-1988) (ABIN153507) anti-Ataxia Telangiectasia Mutated (ATM) (AA 1974-1988) antibody
General 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).

Bartkova, Horejsí, 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).

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).

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).

Bakkenist, Kastan: "DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation." in: Nature, Vol. 421, Issue 6922, pp. 499-506, 2003 (PubMed).

Catalog No. ABIN153507

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