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journal.pone.0289304.pdf | 2.82 MB | Adobe PDF | 見る/開く |
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DCフィールド | 値 | 言語 |
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dc.contributor.author | Hara, Tomohiko | en |
dc.contributor.author | Nakaoka, Hidenori | en |
dc.contributor.author | Miyoshi, Tomoicihiro | en |
dc.contributor.author | Ishikawa, Fuyuki | en |
dc.contributor.alternative | 原, 智彦 | ja |
dc.contributor.alternative | 中岡, 秀憲 | ja |
dc.contributor.alternative | 三好, 知一郎 | ja |
dc.contributor.alternative | 石川, 冬木 | ja |
dc.date.accessioned | 2024-01-04T07:51:48Z | - |
dc.date.available | 2024-01-04T07:51:48Z | - |
dc.date.issued | 2023-08 | - |
dc.identifier.uri | http://hdl.handle.net/2433/286526 | - |
dc.description.abstract | Genomic DNA is constantly exposed to a variety of genotoxic stresses, and it is crucial for organisms to be equipped with mechanisms for repairing the damaged genome. Previously, it was demonstrated that the mammalian CST (CTC1-STN1-TEN1) complex, which was originally identified as a single-stranded DNA-binding trimeric protein complex essential for telomere maintenance, is required for survival in response to hydroxyurea (HU), which induces DNA replication fork stalling. It is still unclear, however, how the CST complex is involved in the repair of diverse types of DNA damage induced by oxidizing agents such as H₂O₂. STN1 knockdown (KD) sensitized HeLa cells to high doses of H₂O₂. While H₂O₂ induced DNA strand breaks throughout the cell cycle, STN1 KD cells were as resistant as control cells to H₂O₂ treatment when challenged in the G1 phase of the cell cycle, but they were sensitive when exposed to H₂O₂ in S/G2/M phase. STN1 KD cells showed a failure of DNA synthesis and RAD51 foci formation upon H₂O₂ treatment. Chemical inhibition of RAD51 in shSTN1 cells did not exacerbate the sensitivity to H₂O₂, implying that the CST complex and RAD51 act in the same pathway. Collectively, our results suggest that the CST complex is required for maintaining genomic stability in response to oxidative DNA damage, possibly through RAD51-dependent DNA repair/protection mechanisms. | en |
dc.language.iso | eng | - |
dc.publisher | Public Library of Science (PLoS) | en |
dc.rights | © 2023 Hara et al. | en |
dc.rights | This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. | en |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | - |
dc.subject | DNA damage | en |
dc.subject | DNA replication | en |
dc.subject | Synthesis phase | en |
dc.subject | HeLa cells | en |
dc.subject | DNA repair | en |
dc.subject | Cell cycle and cell division | en |
dc.subject | Cell staining | en |
dc.subject | Flow cytometry | en |
dc.title | The CST complex facilitates cell survival under oxidative genotoxic stress | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.jtitle | PLOS ONE | en |
dc.identifier.volume | 18 | - |
dc.identifier.issue | 8 | - |
dc.relation.doi | 10.1371/journal.pone.0289304 | - |
dc.textversion | publisher | - |
dc.identifier.artnum | e0289304 | - |
dc.identifier.pmid | 37590191 | - |
dcterms.accessRights | open access | - |
datacite.awardNumber | 19H05655 | - |
datacite.awardNumber | 21K19219 | - |
datacite.awardNumber | 22H02600 | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-19H05655/ | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21K19219/ | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22H02600/ | - |
dc.identifier.eissn | 1932-6203 | - |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.awardTitle | 微小環境変動に対する細胞応答に着目した治癒をめざした抗腫瘍療法 | ja |
jpcoar.awardTitle | ノンコーディング配列Aluレトロトランスポゾンの転移制御因子の探索 | ja |
jpcoar.awardTitle | ゲノム破壊と創生サイクルを生み出すヒトLINE-1の制御機構の解明 | ja |
出現コレクション: | 学術雑誌掲載論文等 |
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