WEKO3
アイテム
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Genetic defects in SAPK signalling, chromatin regulation, vesicle transport and CoA-related lipid metabolism are rescued by rapamycin in fission yeast
https://oist.repo.nii.ac.jp/records/670
https://oist.repo.nii.ac.jp/records/670d92f998f-0bd5-4c7b-b1ac-97a74b264039
名前 / ファイル | ライセンス | アクション |
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Open Biology(Sajiki) (4.5 MB)
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Creative Commons Attribution 4.0 International
https://creativecommons.org/licenses/by/4.0/ |
Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2018-08-15 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Genetic defects in SAPK signalling, chromatin regulation, vesicle transport and CoA-related lipid metabolism are rescued by rapamycin in fission yeast | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者(英) |
Sajiki, Kenichi
× Sajiki, Kenichi× Tahara, Yuria× Villar-Briones, Alejandro× Pluskal, Tomáš× Teruya, Takayuki× Mori, Ayaka× Hatanaka, Mitsuko× Ebe, Masahiro× Nakamura, Takahiro× Aoki, Keita× Nakaseko, Yukinobu× Yanagida, Mitsuhiro |
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書誌情報 |
en : Open Biology 巻 8, p. 170261, 発行日 2018-03-28 |
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抄録 | ||||||
内容記述タイプ | Other | |||||
内容記述 | Rapamycin inhibits TOR (target of rapamycin) kinase, and is being used clinically to treat various diseases ranging from cancers to fibrodysplasia ossificans progressiva. To understand rapamycin mechanisms of action more comprehensively, 1014 temperature-sensitive (ts) fission yeast (Schizosaccharomyces pombe) mutants were screened in order to isolate strains in which the ts phenotype was rescued by rapamycin. Rapamycin-rescued 45 strains, among which 12 genes responsible for temperature sensitivity were identified. These genes are involved in stress-activated protein kinase (SAPK) signalling, chromatin regulation, vesicle transport, and CoA- and mevalonate-related lipid metabolism. Subsequent metabolome analyses revealed that rapamycin upregulated stress-responsive metabolites, while it downregulated purine biosynthesis intermediates and nucleotide derivatives. Rapamycin alleviated abnormalities in cell growth and cell division caused by sty1 mutants (Δsty1) of SAPK. Notably, in Δsty1, rapamycin reduced greater than 75% of overproduced metabolites (greater than 2× WT), like purine biosynthesis intermediates and nucleotide derivatives, to WT levels. This suggests that these compounds may be the points at which the SAPK/TOR balance regulates continuous cell proliferation. Rapamycin might be therapeutically useful for specific defects of these gene functions. | |||||
出版者 | ||||||
出版者 | The Royal Society | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 2046-2441 | |||||
PubMed番号 | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | PMID | |||||
関連識別子 | info:pmid/29593117 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | info:doi/10.1098/rsob.170261 | |||||
権利 | ||||||
権利情報 | © 2018 The Author(s). | |||||
関連サイト | ||||||
識別子タイプ | URI | |||||
関連識別子 | http://rsob.royalsocietypublishing.org/content/8/3/170261 | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |