The telomerase reverse transcriptase regulates chromatin state and DNA damage responses

DOI Web Site 被引用文献8件
  • Kenkichi Masutomi
    Departments of Medical Oncology and Biostatistical Science, Dana–Farber Cancer Institute, Boston, MA 02115; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115; Department of Medicine, Harvard Medical School, Boston, MA 02115; Broad Institute of Harvard and Massachusetts Institute of Technology, 320 Charles Street, Cambridge, MA 02139; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and Terry Fox Laboratory, British Columbia Cancer Agency,...
  • Richard Possemato
    Departments of Medical Oncology and Biostatistical Science, Dana–Farber Cancer Institute, Boston, MA 02115; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115; Department of Medicine, Harvard Medical School, Boston, MA 02115; Broad Institute of Harvard and Massachusetts Institute of Technology, 320 Charles Street, Cambridge, MA 02139; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and Terry Fox Laboratory, British Columbia Cancer Agency,...
  • Judy M. Y. Wong
    Departments of Medical Oncology and Biostatistical Science, Dana–Farber Cancer Institute, Boston, MA 02115; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115; Department of Medicine, Harvard Medical School, Boston, MA 02115; Broad Institute of Harvard and Massachusetts Institute of Technology, 320 Charles Street, Cambridge, MA 02139; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and Terry Fox Laboratory, British Columbia Cancer Agency,...
  • Jennifer L. Currier
    Departments of Medical Oncology and Biostatistical Science, Dana–Farber Cancer Institute, Boston, MA 02115; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115; Department of Medicine, Harvard Medical School, Boston, MA 02115; Broad Institute of Harvard and Massachusetts Institute of Technology, 320 Charles Street, Cambridge, MA 02139; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and Terry Fox Laboratory, British Columbia Cancer Agency,...
  • Zuzana Tothova
    Departments of Medical Oncology and Biostatistical Science, Dana–Farber Cancer Institute, Boston, MA 02115; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115; Department of Medicine, Harvard Medical School, Boston, MA 02115; Broad Institute of Harvard and Massachusetts Institute of Technology, 320 Charles Street, Cambridge, MA 02139; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and Terry Fox Laboratory, British Columbia Cancer Agency,...
  • Judith B. Manola
    Departments of Medical Oncology and Biostatistical Science, Dana–Farber Cancer Institute, Boston, MA 02115; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115; Department of Medicine, Harvard Medical School, Boston, MA 02115; Broad Institute of Harvard and Massachusetts Institute of Technology, 320 Charles Street, Cambridge, MA 02139; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and Terry Fox Laboratory, British Columbia Cancer Agency,...
  • Shridar Ganesan
    Departments of Medical Oncology and Biostatistical Science, Dana–Farber Cancer Institute, Boston, MA 02115; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115; Department of Medicine, Harvard Medical School, Boston, MA 02115; Broad Institute of Harvard and Massachusetts Institute of Technology, 320 Charles Street, Cambridge, MA 02139; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and Terry Fox Laboratory, British Columbia Cancer Agency,...
  • Peter M. Lansdorp
    Departments of Medical Oncology and Biostatistical Science, Dana–Farber Cancer Institute, Boston, MA 02115; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115; Department of Medicine, Harvard Medical School, Boston, MA 02115; Broad Institute of Harvard and Massachusetts Institute of Technology, 320 Charles Street, Cambridge, MA 02139; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and Terry Fox Laboratory, British Columbia Cancer Agency,...
  • Kathleen Collins
    Departments of Medical Oncology and Biostatistical Science, Dana–Farber Cancer Institute, Boston, MA 02115; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115; Department of Medicine, Harvard Medical School, Boston, MA 02115; Broad Institute of Harvard and Massachusetts Institute of Technology, 320 Charles Street, Cambridge, MA 02139; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and Terry Fox Laboratory, British Columbia Cancer Agency,...
  • William C. Hahn
    Departments of Medical Oncology and Biostatistical Science, Dana–Farber Cancer Institute, Boston, MA 02115; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115; Department of Medicine, Harvard Medical School, Boston, MA 02115; Broad Institute of Harvard and Massachusetts Institute of Technology, 320 Charles Street, Cambridge, MA 02139; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and Terry Fox Laboratory, British Columbia Cancer Agency,...

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<jats:p>Constitutive expression of telomerase prevents senescence and crisis by maintaining telomere homeostasis. However, recent evidence suggests that telomerase is dynamically regulated in normal cells and also contributes to transformation independently of net telomere elongation. Here, we show that suppression of the telomerase catalytic subunit [human telomerase reverse transcriptase (hTERT)] expression abrogates the cellular response to DNA double strand breaks. Loss of hTERT does not alter short-term telomere integrity but instead affects the overall configuration of chromatin. Cells lacking hTERT exhibit increased radiosensitivity, diminished capacity for DNA repair, and fragmented chromosomes, demonstrating that loss of hTERT impairs the DNA damage response.</jats:p>

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