• Product nameAnti-ATM antibody [3E8]
    See all ATM primary antibodies
  • Description
    Mouse monoclonal [3E8] to ATM
  • Tested applicationsWB, IPmore details
  • Species reactivity
    Reacts with: Mouse, Rat, Human, Monkey
  • Immunogen

    Recombinant human ATM protein fragmentexpressed in E. coli.

  • Positive control
    • HeLa, Raji or Akata whole cell lysate.



Our Abpromise guarantee covers the use of ab2617 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
  • Application notesIP: Use at a concentration of 2 - 10 µg/ml.
    WB: Use at a concentration of 1 - 2 µg/ml. Predicted molecular weight: 350 kDa.
    This antibody can also be used in an IP-Kinase assay (4)

    Not yet tested in other applications.
    Optimal dilutions/concentrations should be determined by the end user.
  • Target

    • FunctionSerine/threonine protein kinase which activates checkpoint signaling upon double strand breaks (DSBs), apoptosis and genotoxic stresses such as ionizing ultraviolet A light (UVA), thereby acting as a DNA damage sensor. Recognizes the substrate consensus sequence [ST]-Q. Phosphorylates 'Ser-139' of histone variant H2AX/H2AFX at double strand breaks (DSBs), thereby regulating DNA damage response mechanism. Also plays a role in pre-B cell allelic exclusion, a process leading to expression of a single immunoglobulin heavy chain allele to enforce clonality and monospecific recognition by the B-cell antigen receptor (BCR) expressed on individual B lymphocytes. After the introduction of DNA breaks by the RAG complex on one immunoglobulin allele, acts by mediating a repositioning of the second allele to pericentromeric heterochromatin, preventing accessibility to the RAG complex and recombination of the second allele. Also involved in signal transduction and cell cycle control. May function as a tumor suppressor. Necessary for activation of ABL1 and SAPK. Phosphorylates p53/TP53, FANCD2, NFKBIA, BRCA1, CTIP, nibrin (NBN), TERF1, RAD9 and DCLRE1C. May play a role in vesicle and/or protein transport. Could play a role in T-cell development, gonad and neurological function. Plays a role in replication-dependent histone mRNA degradation. Binds DNA ends.
    • Tissue specificityFound in pancreas, kidney, skeletal muscle, liver, lung, placenta, brain, heart, spleen, thymus, testis, ovary, small intestine, colon and leukocytes.
    • Involvement in diseaseDefects in ATM are the cause of ataxia telangiectasia (AT) [MIM:208900]; also known as Louis-Bar syndrome, which includes four complementation groups: A, C, D and E. This rare recessive disorder is characterized by progressive cerebellar ataxia, dilation of the blood vessels in the conjunctiva and eyeballs, immunodeficiency, growth retardation and sexual immaturity. AT patients have a strong predisposition to cancer; about 30% of patients develop tumors, particularly lymphomas and leukemias. Cells from affected individuals are highly sensitive to damage by ionizing radiation and resistant to inhibition of DNA synthesis following irradiation.
      Note=Defects in ATM contribute to T-cell acute lymphoblastic leukemia (TALL) and T-prolymphocytic leukemia (TPLL). TPLL is characterized by a high white blood cell count, with a predominance of prolymphocytes, marked splenomegaly, lymphadenopathy, skin lesions and serous effusion. The clinical course is highly aggressive, with poor response to chemotherapy and short survival time. TPLL occurs both in adults as a sporadic disease and in younger AT patients.
      Note=Defects in ATM contribute to B-cell non-Hodgkin lymphomas (BNHL), including mantle cell lymphoma (MCL).
      Note=Defects in ATM contribute to B-cell chronic lymphocytic leukemia (BCLL). BCLL is the commonest form of leukemia in the elderly. It is characterized by the accumulation of mature CD5+ B lymphocytes, lymphadenopathy, immunodeficiency and bone marrow failure.
    • Sequence similaritiesBelongs to the PI3/PI4-kinase family. ATM subfamily.
      Contains 1 FAT domain.
      Contains 1 FATC domain.
      Contains 1 PI3K/PI4K domain.
    • DomainThe FATC domain is required for interaction with KAT5.
    • Post-translational
      Phosphorylated by NUAK1/ARK5. Autophosphorylation on Ser-367, Ser-1893, Ser-1981 correlates with DNA damage-mediated activation of the kinase.
      Acetylation, on DNA damage, is required for activation of the kinase activity, dimer-monomer transition, and subsequent autophosphorylation on Ser-1981. Acetylated in vitro by KAT5/TIP60.
    • Cellular localizationNucleus. Cytoplasmic vesicle. Primarily nuclear. Found also in endocytic vesicles in association with beta-adaptin.
    • Information by UniProt
    • Database links
    • Alternative names
      • A-T mutated antibody
      • A-T mutated homolog antibody
      • AT mutated antibody
      • AT1 antibody
      • ATA antibody
      • Ataxia telangiectasia mutated antibody
      • Ataxia telangiectasia mutated gene antibody
      • Ataxia telangiectasia mutated homolog (human) antibody
      • Ataxia telangiectasia mutated homolog antibody
      • ATC antibody
      • ATD antibody
      • ATDC antibody
      • ATE antibody
      • ATM antibody
      • ATM serine/threonine kinase antibody
      • ATM_HUMAN antibody
      • DKFZp781A0353 antibody
      • MGC74674 antibody
      • OTTHUMP00000232981 antibody
      • Serine protein kinase ATM antibody
      • Serine-protein kinase ATM antibody
      • Serine/threonine-protein kinase ATM antibody
      • Tefu antibody
      • TEL1 antibody
      • TEL1, telomere maintenance 1, homolog antibody
      • TELO1 antibody
      • Telomere fusion protein antibody
      see all

    References for Anti-ATM antibody [3E8] (ab2617)

    This product has been referenced in:
    • Fernández-Medarde A  et al. RasGRF1 disruption causes retinal photoreception defects and associated transcriptomic alterations. J Neurochem 110:641-52 (2009). Read more (PubMed: 19457086) »
    • Kennedy RD  et al. Fanconi anemia pathway-deficient tumor cells are hypersensitive to inhibition of ataxia telangiectasia mutated. J Clin Invest 117:1440-9 (2007). Read more (PubMed: 17431503) »

    See all 2 Publications for this product

    Product Wall

    There are currently no Abreviews or Questions for ab2617.
    Please use the links above to contact us or submit feedback about this product.