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  1. 福島医学会
  2. Fukushima Journal of Medical Science
  3. Vol.61 (2015)

Overexpression of both CLOCK and BMAL1 inhibits entry to S phase in human colon cancer cells

https://fmu.repo.nii.ac.jp/records/2001902
https://fmu.repo.nii.ac.jp/records/2001902
a7661083-8e82-4295-acbc-fad96493aa47
名前 / ファイル ライセンス アクション
FksmJMedSci_61_p111.pdf FksmJMedSci_61_p111.pdf (1.8 MB)
Item type デフォルトアイテムタイプ(フル)fmu(1)
公開日 2015-12-25
タイトル
タイトル Overexpression of both CLOCK and BMAL1 inhibits entry to S phase in human colon cancer cells
言語 en
作成者 Sakamoto, Wataru

× Sakamoto, Wataru

en Sakamoto, Wataru

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Takenoshita, Seiichi

× Takenoshita, Seiichi

en Takenoshita, Seiichi

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権利情報
権利情報 © 2015 The Fukushima Society of Medical Science
内容記述
内容記述タイプ Abstract
内容記述 Many physiological, biochemical and behavioral processes operate under the circadian rhythm, which is generated by an internal time-keeping mechanism commonly referred to as the biological clock, in almost all organisms from bacteria to mammals. The core circadian oscillator is composed of an autoregulatory transcription-translation feedback loop, in which CLOCK and BMAL1 are positive regulators. A cell has two mechanisms, "cell cycle" and "cell rhythm", the relationship between which remains controversial. Therefore, the aim of this study was to explore the effect of Clock and Bmal1 on cell cycle, especially on the G1 phase, using vectors with the tetracycline operator-repressor system. The present study revealed that simultaneous induction of Bmal1 and Clock had an influential effect on the cell cycle in SW480/T-REx/Clock/Bmal1 cells, in which both Clock and Bmal1 could be induced by tetracycline. The observation that induction of both Clock and Bmal1 inhibited cell growth and the significant increase of the G1 phase proportion of in SW480/T-REx/Clock/Bmal1 cells indicated that entry from the G1 to S phase was inhibited by the induction of Clock and Bmal1. Furthermore, overexpression of Clock and Bmal1 prevented the cells from entering into the G2/M phase induced by Paclitaxel, and made the cells more resistant to the agent. In conclusion, we found that overexpression of both Clock and Bmal1 suppressed cell growth. In addition, the present study raised the possibility that Clock and Bmal1 may in part play a role in preventing the cells from entering G1 to S phase of cell cycle via suppression of CyclinD1 expression, and thus acquiring resistance to Paclitaxel.
出版者
出版者 The Fukushima Society of Medical Science
言語
言語 eng
書誌情報 en : Fukushima Journal of Medical Science

巻 61, 号 2, p. 111-124, 発行日 2015
関連情報
関連タイプ isIdenticalTo
識別子タイプ DOI
関連識別子 https://doi.org/10.5387/fms.2015-11
関連情報
識別子タイプ PMID
関連識別子 26370682
関連情報
識別子タイプ ICHUSHI
関連識別子 2017088014
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
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
収録物識別子
収録物識別子タイプ PISSN
収録物識別子 0016-2590
収録物識別子
収録物識別子タイプ EISSN
収録物識別子 2185-4610
収録物識別子
収録物識別子タイプ NCID
収録物識別子 AA0065246X
主題
主題Scheme Other
主題 circadian rhythm
主題
主題Scheme Other
主題 Clock
主題
主題Scheme Other
主題 Bmal1
主題
主題Scheme Other
主題 cell cycle
主題
主題Scheme Other
主題 paclitaxel
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