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ATM prevents the persistence and propagation of chromosome breaks in lymphocytes.

ATM prevents the persistence and propagation of chromosome breaks in lymphocytes. Research Abstract Details 

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  • ATM prevents the persistence and propagation of chromosome breaks in lymphocytes. Abstract Text:

    elsa Elsa ,mila jankovicMila Jankovic,simone difilippantonioSimone Difilippantonio,jeremy a danielJeremy A Daniel,hua-tang chenHua-Tang Chen,arkady celesteArkady Celeste,manuela pellegriniManuela Pellegrini,kevin mcbrideKevin McBride,danny wangsaDanny Wangsa,andrea l bredemeyerAndrea L Bredemeyer,barry p sleckmanBarry P Sleckman,thomas riedThomas Ried,michel nussenzweigMichel Nussenzweig, nussenzweig Nussenzweig,

    DNA double-strand breaks (DSBs) induce a signal transmitted by the ataxia-telangiectasia mutated (ATM) kinase, which suppresses illegitimate joining of DSBs and activates cell-cycle checkpoints. Here we show that a significant fraction of mature ATM-deficient lymphocytes contain telomere-deleted ends produced by failed end joining during V(D)J recombination. These RAG-1/2 endonuclease-dependent, terminally deleted chromosomes persist in peripheral lymphocytes for at least 2 weeks in vivo and are stable over several generations in vitro. Restoration of ATM kinase activity in mature lymphocytes that have transiently lost ATM function leads to loss of cells with terminally deleted chromosomes. Thus, maintenance of genomic stability in lymphocytes requires faithful end joining as well a checkpoint that prevents the long-term persistence and transmission of DSBs. Silencing this checkpoint permits DNA ends produced by V(D)J recombination in a lymphoid precursor to serve as substrates for translocations with chromosomes subsequently damaged by other means in mature cells.

    ATM prevents the persistence and propagation of chromosome breaks in lymphocytes. Publishing Authors By Initials

    e E ,m jankovicM Jankovic,s difilippantonioS Difilippantonio,ja danielJA Daniel,ht chenHT Chen,a celesteA Celeste,m pellegriniM Pellegrini,k mcbrideK McBride,d wangsaD Wangsa,al bredemeyerAL Bredemeyer,bp sleckmanBP Sleckman,t riedT Ried,m nussenzweigM Nussenzweig,a nussenzweigA Nussenzweig,

    For similar proteins: neoplasm proteins: tumor suppressor proteins research abstracts see: proteins: neoplasm proteins: tumor suppressor proteins research

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    ATM prevents the persistence and propagation of chromosome breaks in lymphocytes. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Cell

    VOLUME: 130

    Page Numbers: 63-75

    Journal Abbreviation: Cell

    ISSN: 0092-8674

    DAY: 28

    MONTH: 06

    YEAR: 2007

    ATM prevents the persistence and propagation of chromosome breaks in lymphocytes. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 413066

    ATM prevents the persistence and propagation of chromosome breaks in lymphocytes. Keywords Mesh Terms:

    KEYWORDS: Tumor Suppressor Proteins

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: ATM prevents the persistence and propagation of chromosome breaks in lymphocytes. Information

    Substance Name: Protein-Serine-Threonine Kinases

    Registry Number: EC 2.7.11.1

    Grant and Affiliation Information for ATM prevents the persistence and propagation of chromosome breaks in lymphocytes.

    AFFILIATION: Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-1360, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: Cell

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