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- Hashimoto Hiroshi
- School of Pharmaceutical Sciences, University of Shizuoka
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- Hishiki Asami
- School of Pharmaceutical Sciences, University of Shizuoka
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- Hara Kodai
- School of Pharmaceutical Sciences, University of Shizuoka
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- Kikuchi Sotaro
- School of Pharmaceutical Sciences, University of Shizuoka Department of Pharmacology, University of Texas Southwestern Medical Center
抄録
<p>DNA damage tolerance (DDT) is a cell function to avoid replication arrest by DNA damage during DNA replication. DDT includes two pathways, translesion DNA synthesis (TLS) and template-switched DNA synthesis (TS). DDT is regulated by ubiquitination of proliferating cell nuclear antigen that binds to double-stranded DNA and functions as scaffold protein for DNA metabolism. TLS is transient DNA synthesis using damaged DNA as a template by error-prone DNA polymerases termed TLS polymerases specialized for DNA damage. TS, in which one newly synthesized strand is utilized as an undamaged template for replication by replicative polymerases, is error-free process. Thus, DDT is not inherently a repair pathway. DDT is a mechanism to tolerate DNA damage, giving priority to DNA synthesis and enabling finish of DNA replication for cell survival and genome stability. DDT is associated with cancer development and thus is of great interest in drug discovery for cancer therapy. This review article describes recent progress in structural studies on protein-protein and protein-DNA complexes involved in TLS and TS, providing the molecular mechanisms of interactions in DDT.</p>
収録刊行物
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- Biophysics and Physicobiology
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Biophysics and Physicobiology 14 (0), 199-205, 2017
一般社団法人 日本生物物理学会
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詳細情報 詳細情報について
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- CRID
- 1390282680741104128
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- NII論文ID
- 130006269291
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- ISSN
- 21894779
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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
- Crossref
- CiNii Articles
- KAKEN
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- 抄録ライセンスフラグ
- 使用不可