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
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- SATO Koichiro
- Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
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- KIBE Tatsuya
- Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University Department of Chemistry, Shizuoka University
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- SEIMIYA Hiroyuki
- Division of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research
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- NAKAMURA Asako
- Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health
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- YUKAWA Masashi
- Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
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- TSUCHIYA Eiko
- Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
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- UENO Masaru
- Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
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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.
収録刊行物
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- Bioscience, Biotechnology, and Biochemistry
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Bioscience, Biotechnology, and Biochemistry 74 (2), 382-385, 2010
公益社団法人 日本農芸化学会
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詳細情報 詳細情報について
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- CRID
- 1390282681454256000
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- NII論文ID
- 10027551727
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- NII書誌ID
- AA10824164
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- ISSN
- 13476947
- 09168451
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- NDL書誌ID
- 10580106
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
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- 使用不可