05-740 | Anti-phospho-ATM (Ser1981) Antibody, clone 10H11.E12

05-740
200 µg  
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      Overview

      Replacement Information

      Key Spec Table

      Species ReactivityKey ApplicationsHostFormatAntibody Type
      H, MICC, IF, IP, WBMPurifiedMonoclonal Antibody
      Description
      Catalogue Number05-740
      Brand Family Upstate
      Trade Name
      • Upstate
      DescriptionAnti-phospho-ATM (Ser1981) Antibody, clone 10H11.E12
      Alternate Names
      • A-T, mutated
      • AT mutated
      • TEL1
      • telomere maintenance 1, homolog
      • ataxia telangiectasia mutated
      • ataxia telangiectasia mutated (includes complementation groups A, C and D)
      • ataxia telangiectasia mutated protein
      • human phosphatidylinositol 3-kinase homolog
      • serine-protein kinase ATM
      Background InformationAtaxia telangiectasia mutated kinase (ATM) and ataxia telangiectasia and Rad3-related kinase (ATR) are related kinases that regulate cell cycle checkpoints and DNA repair. Mutation in the ATM gene results in the autosomal recessive disease ataxia telangiectasia (AT). The identified substrates for ATM are p53, p95/NBS1, MDM2, Chk2, BRCA1, CtIP, 4E-BP1 and Chk1. The essential requirement for the substrates of ATM/ATR is S/TQ. Hydrophobic amino acids at positions -3 and -1, and negatively charged amino acids at position +1 are positive determinants for substrate recognition by these kinases. Positively charged residues surrounding the S/TQ are negative determinants for substrate phosphorylation. The complex phenotype of cells derived from patients with AT suggests that ATM has additional cellular substrates. In unirradiated cells, ATM is present as an inactive homodimer or multimer. Double-stranded breaks in DNA caused by ionizing radiation cause rapid ATM kinase activation through dissociation of this complex and ATM autophosphorylation at Ser1981.
      References
      Product Information
      FormatPurified
      Control
      • Irradiated HeLa cell lysates
      PresentationProtein G purified mouse IgG in 0.014 M phosphate buffer, pH 7.6, with 0.175 M NaCl, 0.07 % Sodium Azide and 30% glycerol. Liquid at -20°C.
      Applications
      ApplicationUse Anti-phospho-ATM (Ser1981) Antibody, clone 10H11.E12 (Mouse Monoclonal Antibody) validated in ICC, IF, IP, WB to detect phospho-ATM (Ser1981) also known as A-T mutated.
      Key Applications
      • Immunocytochemistry
      • Immunofluorescence
      • Immunoprecipitation
      • Western Blotting
      Application NotesImmunoprecipitation:
      Phosphorylated ATM was immunoprecipitated from irradiated HeLa cells (Figure A, lanes 3 and 4).

      Immunocytochemistry:
      Foci are detected in irradiated human and mouse fibroblasts. Determined by an independent laboratory.
      Biological Information
      ImmunogenKLH-conjugated, synthetic peptide corresponding to amino acids 1974-1988 (SLAFEEG[pS]QSTTISS) of human ATM. The immunizing sequence has 11/12 identical amino acids in mouse and rat.
      Clone10H11.E12
      ConcentrationPlease refer to the Certificate of Analysis for the lot-specific concentration.
      HostMouse
      SpecificityThis antibody recognizes ATM, Mr ~370 kDa. A non-specific protein was also detected, Mr ~ >400 kDa.
      IsotypeIgG1κ
      Species Reactivity
      • Human
      • Mouse
      Species Reactivity NoteHuman and mouse. Predicted to cross-react with rat based on sequence homology
      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
      Modifications
      • Phosphorylation
      Purification MethodProtein G Purified
      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 Weight~370 kDa
      Physicochemical Information
      Dimensions
      Materials Information
      Toxicological Information
      Safety Information according to GHS
      Safety Information
      Product Usage Statements
      Quality AssuranceRoutinely evaluated by immunoblot on in crude lysates from irradiated HeLa cells.

      Western Blot Analysis:
      0.5 µg/mL of this lot detected phosphorylated ATM in crude lysates from irradiated HeLa 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 ConditionsStable for 1 year at -20°C from date of receipt.

      Handling Recommendations:
      Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance. Note: Variability in freezer temperatures below -20°C may cause glycerol containing solutions to become frozen during storage.
      Packaging Information
      Material Size200 µg
      Transport Information
      Supplemental Information
      Specifications

      Documentation

      SDS

      Title

      Safety Data Sheet (SDS) 

      Certificates of Analysis

      TitleLot Number
      Anti-phospho-ATM (Ser1981) clone 10H11.E12 (mouse monoclonal) Monoclonal Antibody Q2909941
      Anti-phospho-ATM (Ser1981), clone 10H11.E12 - 2144400 2144400
      Anti-phospho-ATM (Ser1981), clone 10H11.E12 - 2383524 2383524
      Anti-phospho-ATM (Ser1981), clone 10H11.E12 - 2464600 2464600
      Anti-phospho-ATM (Ser1981), -2524628 2524628
      Anti-phospho-ATM (Ser1981), -2593886 2593886
      Anti-phospho-ATM (Ser1981), -2617637 2617637
      Anti-phospho-ATM (Ser1981), -2649118 2649118
      Anti-phospho-ATM (Ser1981), -2700801 2700801
      Anti-phospho-ATM (Ser1981), -2727301 2727301

      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
      The DNA damage/repair cascade in glioblastoma cell lines after chemotherapeutic agent treatment.
      Annovazzi, L; Caldera, V; Mellai, M; Riganti, C; Battaglia, L; Chirio, D; Melcarne, A; Schiffer, D
      International journal of oncology  46  2299-308  2015

      Show Abstract
      25892134 25892134
      Characterization of LGALS3 (galectin-3) as a player in DNA damage response.
      Carvalho, RS; Fernandes, VC; Nepomuceno, TC; Rodrigues, DC; Woods, NT; Suarez-Kurtz, G; Chammas, R; Monteiro, AN; Carvalho, MA
      Cancer biology & therapy  15  840-50  2014

      Show Abstract
      24755837 24755837
      Wild-type p53-induced phosphatase 1 (Wip1) forestalls cellular premature senescence at physiological oxygen levels by regulating DNA damage response signaling during DNA replication.
      Sakai, H; Fujigaki, H; Mazur, SJ; Appella, E
      Cell cycle (Georgetown, Tex.)  13  1015-29  2014

      Show Abstract
      Immunocytochemistry24552809 24552809
      A novel interplay between the Fanconi anemia core complex and ATR-ATRIP kinase during DNA cross-link repair.
      Tomida, J; Itaya, A; Shigechi, T; Unno, J; Uchida, E; Ikura, M; Masuda, Y; Matsuda, S; Adachi, J; Kobayashi, M; Meetei, AR; Maehara, Y; Yamamoto, K; Kamiya, K; Matsuura, A; Matsuda, T; Ikura, T; Ishiai, M; Takata, M
      Nucleic acids research  41  6930-41  2013

      Show Abstract
      23723247 23723247
      DNA damage enhances integration of HIV-1 into macrophages by overcoming integrase inhibition.
      Koyama, T; Sun, B; Tokunaga, K; Tatsumi, M; Ishizaka, Y
      Retrovirology  10  21  2013

      Show Abstract
      23432899 23432899
      Zinc finger protein 668 interacts with Tip60 to promote H2AX acetylation after DNA damage.
      Hu, R; Wang, E; Peng, G; Dai, H; Lin, SY
      Cell cycle (Georgetown, Tex.)  12  2033-41  2013

      Show Abstract
      23777805 23777805
      Resistance to DNA-damaging treatment in non-small cell lung cancer tumor-initiating cells involves reduced DNA-PK/ATM activation and diminished cell cycle arrest.
      Lundholm, L; Hååg, P; Zong, D; Juntti, T; Mörk, B; Lewensohn, R; Viktorsson, K
      Cell death & disease  4  e478  2013

      Show Abstract
      23370278 23370278
      Activation-induced cytidine deaminase-initiated off-target DNA breaks are detected and resolved during S phase.
      Hasham, MG; Snow, KJ; Donghia, NM; Branca, JA; Lessard, MD; Stavnezer, J; Shopland, LS; Mills, KD
      Journal of immunology (Baltimore, Md. : 1950)  189  2374-82  2012

      Show Abstract
      22826323 22826323
      Role of the translationally controlled tumor protein in DNA damage sensing and repair.
      Zhang, J; de Toledo, SM; Pandey, BN; Guo, G; Pain, D; Li, H; Azzam, EI
      Proceedings of the National Academy of Sciences of the United States of America  109  E926-33  2012

      Show Abstract
      22451927 22451927

      Brochure

      Title
      Product Selection Guide - Antibodies, small molecule inhibitors, kits, assays and proteins for signaling research.
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      Categories

      Life Science Research > Antibodies and Assays > Primary Antibodies