Expression of Mutant RPA in Human Cancer Cells Causes Telomere Shortening

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  • KOBAYASHI Yuka
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • SATO Koichiro
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • KIBE Tatsuya
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University Department of Chemistry, Shizuoka University
  • SEIMIYA Hiroyuki
    Division of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research
  • NAKAMURA Asako
    Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health
  • YUKAWA Masashi
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • TSUCHIYA Eiko
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • UENO Masaru
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University

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Abstract

Replication protein A (RPA) binds to single-stranded DNA generated during DNA replication and other processes. The roles of RPA in telomere maintenance have been demonstrated in yeasts, but not in telomerase-positive human cells. In this study, we found that expression of mutant RPA70 in human cells caused telomere shortening, suggesting that RPA is required for telomere-length regulation in human cancer cells.

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