05-513 | Anti-ATM Antibody, clone AM9

05-513
200 µL  
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      Overview

      Replacement Information

      Key Spec Table

      Species ReactivityKey ApplicationsHostFormatAntibody Type
      HWBMAscitesMonoclonal Antibody
      Description
      Catalogue Number05-513
      Replaces04-200
      Brand Family Upstate
      Trade Name
      • Upstate
      DescriptionAnti-ATM Antibody, clone AM9
      References
      Product Information
      FormatAscites
      Presentationmouse ascites containing 0.05% sodium azide
      Applications
      ApplicationDetect ATM also known as Ataxia Telangiectasia Mutated with Anti-ATM Antibody, clone AM9 (Mouse Monoclonal Antibody), that has been demonstrated to work in WB.
      Key Applications
      • Western Blotting
      Biological Information
      ImmunogenFull-length human ATM
      Cloneclone AM9
      HostMouse
      SpecificityATM
      IsotypeIgG
      Species Reactivity
      • Human
      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
      • AT
      • TELO1
      • ATC
      • DKFZp781A0353
      • MGC74674
      • ATD
      • ATA
      • AT1
      • T-PLL
      • ATE
      • TEL1
      • ATDC
      • TPLL
      Purification MethodAscites
      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.
      Molecular Weight350kDa
      Physicochemical Information
      Dimensions
      Materials Information
      Toxicological Information
      Safety Information according to GHS
      Safety Information
      Product Usage Statements
      Quality Assuranceroutinely evaluated by immunoblot on nuclear extract from Raji cells
      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 Conditions2 years at -20°C
      Packaging Information
      Material Size200 µL
      Transport Information
      Supplemental Information
      Specifications

      Documentation

      SDS

      Title

      Safety Data Sheet (SDS) 

      Certificates of Analysis

      TitleLot Number
      Anti-ATM, clone AM9 - 18793 18793
      Anti-ATM, clone AM9 - 23560 23560
      Anti-ATM, clone AM9 - 27273 27273
      Anti-ATM, clone AM9 - DAM1794279 DAM1794279
      Anti-ATM, clone AM9 -2575524 2575524
      Anti-ATM, clone AM9 -2691204 2691204
      Anti-ATM, clone AM9 -2697421 2697421
      Anti-ATM, clone AM9 -2829468 2829468
      Anti-ATM, clone AM9 Monoclonal Antibody 2896054

      References

      Reference overviewApplicationPub Med ID
      Mir-23a induces telomere dysfunction and cellular senescence by inhibiting TRF2 expression.
      Luo, Z; Feng, X; Wang, H; Xu, W; Zhao, Y; Ma, W; Jiang, S; Liu, D; Huang, J; Songyang, Z
      Aging cell  14  391-9  2015

      Show Abstract
      25753893 25753893
      Systems-level overview of host protein phosphorylation during Shigella flexneri infection revealed by phosphoproteomics.
      Schmutz, C; Ahrné, E; Kasper, CA; Tschon, T; Sorg, I; Dreier, RF; Schmidt, A; Arrieumerlou, C
      Molecular & cellular proteomics : MCP  12  2952-68  2013

      Show Abstract
      23828894 23828894
      Characterization of mre11 loss following HSV-1 infection.
      Gregory, DA; Bachenheimer, SL
      Virology  373  124-36  2008

      Show Abstract
      18177684 18177684
      ATM is a cytoplasmic protein in mouse brain required to prevent lysosomal accumulation
      Barlow, C, et al
      Proc Natl Acad Sci USA, 97:871-6 (2000)  2000

      10639172 10639172
      Requirement of ATM in phosphorylation of the human p53 protein at serine 15 following DNA double-strand breaks.
      Nakagawa, K, et al.
      Mol. Cell. Biol., 19: 2828-34 (1999)  1999

      Show Abstract
      10082548 10082548
      Radiation-induced assembly of Rad51 and Rad52 recombination complex requires ATM and c-Abl.
      Chen, G, et al.
      J. Biol. Chem., 274: 12748-52 (1999)  1999

      Show Abstract
      Immunoprecipitation10212258 10212258
      Atm inactivation results in aberrant telomere clustering during meiotic prophase.
      Pandita, T K, et al.
      Mol. Cell. Biol., 19: 5096-105 (1999)  1999

      Show Abstract
      10373558 10373558

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      Categories

      Life Science Research > Antibodies and Assays > Primary Antibodies