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dc.contributor.author | Morita, Ken | en |
dc.contributor.author | Noura, Mina | en |
dc.contributor.author | Tokushige, Chieko | en |
dc.contributor.author | Maeda, Shintaro | en |
dc.contributor.author | Kiyose, Hiroki | en |
dc.contributor.author | Kashiwazaki, Gengo | en |
dc.contributor.author | Taniguchi, Junichi | en |
dc.contributor.author | Bando, Toshikazu | en |
dc.contributor.author | Yoshida, Kenichi | en |
dc.contributor.author | Ozaki, Toshifumi | en |
dc.contributor.author | Matsuo, Hidemasa | en |
dc.contributor.author | Ogawa, Seishi | en |
dc.contributor.author | Liu, Pu Paul | en |
dc.contributor.author | Nakahata, Tatsutoshi | en |
dc.contributor.author | Sugiyama, Hiroshi | en |
dc.contributor.author | Adachi, Souichi | en |
dc.contributor.author | Kamikubo, Yasuhiko | en |
dc.contributor.alternative | 森田, 剣 | ja |
dc.contributor.alternative | 能浦, 三奈 | ja |
dc.contributor.alternative | 徳重, 智恵子 | ja |
dc.contributor.alternative | 前田, 信太郎 | ja |
dc.contributor.alternative | 清瀬, 大樹 | ja |
dc.contributor.alternative | 柏﨑, 玄伍 | ja |
dc.contributor.alternative | 谷口, 淳一 | ja |
dc.contributor.alternative | 板東, 俊和 | ja |
dc.contributor.alternative | 吉田, 健一 | ja |
dc.contributor.alternative | 松尾, 英将 | ja |
dc.contributor.alternative | 小川, 誠司 | ja |
dc.contributor.alternative | 中畑, 龍俊 | ja |
dc.contributor.alternative | 杉山, 弘 | ja |
dc.contributor.alternative | 足立, 壯一 | ja |
dc.contributor.alternative | 上久保, 靖彦 | ja |
dc.date.accessioned | 2017-12-04T07:16:41Z | - |
dc.date.available | 2017-12-04T07:16:41Z | - |
dc.date.issued | 2017-11-30 | - |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | http://hdl.handle.net/2433/228155 | - |
dc.description | 急性骨髄性白血病の抗がん剤耐性メカニズム、一部解明. 京都大学プレスリリース. 2017-12-04. | ja |
dc.description.abstract | Although runt-related transcription factor 1 (RUNX1) and its associating core binding factor-β (CBFB) play pivotal roles in leukemogenesis, and inhibition of RUNX1 has now been widely recognized as a novel strategy for anti-leukemic therapies, it has been elusive how leukemic cells could acquire the serious resistance against RUNX1-inhibition therapies and also whether CBFB could participate in this process. Here, we show evidence that p53 (TP53) and CBFB are sequentially up-regulated in response to RUNX1 depletion, and their mutual interaction causes the physiological resistance against chemotherapy for acute myeloid leukemia (AML) cells. Mechanistically, p53 induced by RUNX1 gene silencing directly binds to CBFB promoter and stimulates its transcription as well as its translation, which in turn acts as a platform for the stabilization of RUNX1, thereby creating a compensative RUNX1-p53-CBFB feedback loop. Indeed, AML cells derived from relapsed cases exhibited higher CBFB expression levels compared to those from primary AML cells at diagnosis, and these CBFB expressions were positively correlated to those of p53. Our present results underscore the importance of RUNX1-p53-CBFB regulatory loop in the development and/or maintenance of AML cells, which could be targeted at any sides of this triangle in strategizing anti-leukemia therapies. | en |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Springer Nature | en |
dc.rights | © The Author(s) 2017 | en |
dc.rights | This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. | en |
dc.subject | Acute myeloid leukaemia | en |
dc.subject | Oncogenes | en |
dc.title | Autonomous feedback loop of RUNX1-p53-CBFB in acute myeloid leukemia cells | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.jtitle | Scientific Reports | en |
dc.identifier.volume | 7 | - |
dc.relation.doi | 10.1038/s41598-017-16799-z | - |
dc.textversion | publisher | - |
dc.identifier.artnum | 16604 | - |
dc.identifier.pmid | 29192243 | - |
dc.relation.url | https://www.kyoto-u.ac.jp/ja/research-news/2017-12-04-0 | - |
dcterms.accessRights | open access | - |
出現コレクション: | 学術雑誌掲載論文等 |
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