A part of MilliporeSigma

MAB3806 | Anti-ATM phosphoSer1981 Antibody, clone 10H11.E12

100 µg  
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      Key Specifications Table

      Species ReactivityKey ApplicationsHostFormatAntibody Type
      H, M IP, WB, ICC M Purified Monoclonal Antibody
      Catalogue NumberMAB3806
      Brand Family Chemicon®
      Trade Name
      • Chemicon
      DescriptionAnti-ATM phosphoSer1981 Antibody, clone 10H11.E12
      Alternate Names
      • Ataxia Telangiectasia Mutated
      Background InformationATM is a 370 kDa nuclear phosphoprotein involved in the autosomal recessive disease Ataxia Telangiectasia (AT). Ataxia telangiectasia (AT) is a debilitating neurodegenerative disease that occurs early in childhood, resulting in ataxic movements and speech defects caused by cerebellar degeneration. The underlying cause of the disease is a biochemical dysfunction in the cellular response to specific types of DNA damage, correlated with mutations in the protein kinase ATM (Ataxia telangiectasia mutated). ATM not only is key in the signaling cascade that responds to DNA double-stranded breaks, but it also controls cell-cycle checkpoints and is therefore important in cancer prevention.
      Product Information
      • Irradiated normal Human fibroblasts (no reactivity against non-irradiated cell extracts)
      PresentationPurified immunoglobulin presented as a liquid in 0.02M phosphate buffer containing 0.25M NaCl and 0.1% sodium azide.
      ApplicationAnti-ATM Antibody, phosphoSer1981, clone 10H11.E12 is a Mouse Monoclonal Antibody for detection of ATM also known as Ataxia Telangiectasia Mutated & has been validated in IP, WB, ICC.
      Key Applications
      • Immunoprecipitation
      • Western Blotting
      • Immunocytochemistry
      Application NotesWestern blot: Detects a 370 kDa protein in crude extracts from irradiated human foreskin or mouse 3T3L1 cells.

      Immunocytochemistry: Foci are detected in irradiated human and mouse fibroblasts.

      Immunoprecipitation: The antibody immunoprecipitates ATM from irradiated human and mouse cells.

      Optimal working dilutions must be determined by end user.
      Biological Information
      ImmunogenSynthetic peptide corresponding to amino acids 1974-1988 of human ATM (SLAFEEG[pS]QSTTISS).
      ConcentrationPlease refer to the Certificate of Analysis for the lot-specific concentration.
      SpecificityReacts with ATM Kinase phosphorylated at serine 1981. Clone 10H11.E12 is covered by US patent No. 6,916,627 and 7,108,992.
      Species Reactivity
      • Human
      • Mouse
      Antibody TypeMonoclonal Antibody
      Entrez Gene Number
      Entrez Gene SummaryThe protein encoded by this gene belongs to the PI3/PI4-kinase family. This protein is an important cell cycle checkpoint kinase that phosphorylates; thus, it functions as a regulator of a wide variety of downstream proteins, including tumor suppressor proteins p53 and BRCA1, checkpoint kinase CHK2, checkpoint proteins RAD17 and RAD9, and DNA repair protein NBS1. This protein and the closely related kinase ATR are thought to be master controllers of cell cycle checkpoint signaling pathways that are required for cell response to DNA damage and for genome stability. Mutations in this gene are associated with ataxia telangiectasia, an autosomal recessive disorder. Two transcript variants encoding different isoforms have been found for this gene.
      Gene Symbol
      • ATM
      • ATD
      • AT
      • TELO1
      • ATA
      • AT1
      • ATC
      • T-PLL
      • DKFZp781A0353
      • ATE
      • TEL1
      • ATDC
      • TPLL
      • MGC74674
      • EC
      • Phosphorylation
      UniProt Number
      UniProt SummaryFUNCTION: SwissProt: Q13315 # Serine/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 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.
      SIZE: 3056 amino acids; 350644 Da
      SUBUNIT: Exists in monomeric and tetrameric state. Binds DNA ends, p53/TP53, ABL1, BRCA1, NBN/nibrin and TERF1. Part of the BRCA1- associated genome surveillance complex (BASC), which contains BRCA1, MSH2, MSH6, MLH1, ATM, BLM, PMS2 and the RAD50-MRE11-NBN protein complex. This association could be a dynamic process changing throughout the cell cycle and within subnuclear domains. DNA damage promotes association with RAD17. Interacts with EEF1E1. This interaction, which takes place independently of TP53, is induced by DNA damage that may occur during genotoxic stress or cell growth. Interacts with DCLRE1C. Interacts with MYST1. Interacts with HTATIP.
      SUBCELLULAR LOCATION: Nucleus. Cytoplasmic vesicle. Note=Primarily nuclear. Found also in endocytic vesicles in association with beta-adaptin.
      TISSUE SPECIFICITY: Found in pancreas, kidney, skeletal muscle, liver, lung, placenta, brain, heart, spleen, thymus, testis, ovary, small intestine, colon and leukocytes.DOMAIN:SwissProt: Q13315 The FATC domain is required for interaction with HTATIP.
      PTM: Phosphorylated by ARK5. Autophosphorylated on Ser-1981 upon DNA damage. & Acetylated by HTATIP upon DNA damage; which is required for autophosphorylation and subsequent activation.
      DISEASE: SwissProt: Q13315 # Defects 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. & 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. & Defects in ATM contribute to B-cell non-Hodgkin lymphomas (BNHL), including mantle cell lymphoma (MCL). & 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.
      SIMILARITY: Belongs to the PI3/PI4-kinase family. ATM subfamily. & Contains 1 FAT domain. & Contains 1 FATC domain. & Contains 1 PI3K/PI4K domain.
      Physicochemical Information
      Materials Information
      Toxicological Information
      Safety Information according to GHS
      Safety Information
      Product Usage Statements
      Usage Statement
      • Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
      Storage and Shipping Information
      Storage ConditionsMaintain at 2-8°C in undiluted aliquots for up to 6 months from date of receipt.

      This antibody and certain aspects of its use are disclosed and claimed in pending U.S. Patent Applications published as U.S. Patent Publication Nos. 2003/0077661 and 2003/0157572.
      Packaging Information
      Material Size100 µg
      Transport Information
      Supplemental Information




      Safety Data Sheet (SDS) 

      Certificates of Analysis

      TitleLot Number
      MOUSE ANTI-ATM KINASE phosphoSer 1981 -2701009 2701009
      MOUSE ANTI-ATM KINASE phosphoSer 1981 -2786074 2786074
      MOUSE ANTI-ATM KINASE phosphoSer 1981 MONOCLONAL ANTIBODY - 2455741 2455741
      MOUSE ANTI-ATM KINASE phosphoSer 1981 MONOCLONAL ANTIBODY - 2015985 2015985
      MOUSE ANTI-ATM KINASE phosphoSer 1981 MONOCLONAL ANTIBODY - 2070832 2070832
      MOUSE ANTI-ATM KINASE phosphoSer 1981 MONOCLONAL ANTIBODY - 2234147 2234147
      MOUSE ANTI-ATM KINASE phosphoSer 1981 MONOCLONAL ANTIBODY -2528725 2528725
      MOUSE ANTI-ATM KINASE phosphoSer 1981 MONOCLONAL ANTIBODY -2609839 2609839
      MOUSE ANTI-ATM KINASE phosphoSer 1981 MONOCLONAL ANTIBODY -2628821 2628821
      MOUSE ANTI-ATM KINASE phosphoSer 1981 MONOCLONAL ANTIBODY -2739324 2739324


      Reference overviewPub Med ID
      FOXM1 targets NBS1 to regulate DNA damage-induced senescence and epirubicin resistance.
      Khongkow, P; Karunarathna, U; Khongkow, M; Gong, C; Gomes, AR; Yagüe, E; Monteiro, LJ; Kongsema, M; Zona, S; Man, EP; Tsang, JW; Coombes, RC; Wu, KJ; Khoo, US; Medema, RH; Freire, R; Lam, EW
      Oncogene 33 4144-55 2014

      Show Abstract
      24141789 24141789
      Specific acetylation of p53 by HDAC inhibition prevents DNA damage-induced apoptosis in neurons.
      Brochier, C; Dennis, G; Rivieccio, MA; McLaughlin, K; Coppola, G; Ratan, RR; Langley, B
      The Journal of neuroscience : the official journal of the Society for Neuroscience 33 8621-32 2013

      Show Abstract
      23678107 23678107
      Development of a high-content high-throughput screening assay for the discovery of ATM signaling inhibitors.
      Bardelle, C; Boros, J
      Journal of biomolecular screening 17 912-20 2012

      Show Abstract
      22653913 22653913
      ATM-mediated phosphorylation activates the tumor-suppressive function of B56?-PP2A.
      G P Shouse,Y Nobumori,M J Panowicz,X Liu
      Oncogene 30 2011

      Show Abstract
      21460856 21460856
      DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation.
      Bakkenist, Christopher J and Kastan, Michael B
      Nature, 421: 499-506 (2003) 2003

      Show Abstract
      12556884 12556884

      Data Sheet