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  1. 30 医学部・医学研究科・附属病院
  2. 30b 紀要論文
  3. 30b-01 弘前医学 = Hirosaki Medical Journal
  4. 76巻1-4号

Reciprocal regulatory mechanisms between the integrated stress response pathway and cyclin D1 in the mitochondrial stress response

http://hdl.handle.net/10129/0002001992
http://hdl.handle.net/10129/0002001992
23b152c3-99c8-4861-ba77-f76c543b05df
名前 / ファイル ライセンス アクション
Hirosaki Hirosaki Med J 76-1-4_94.pdf (1.8 MB)
アイテムタイプ リポジトリ登録用アイテムタイプ(フル)(1)
公開日 2026-03-25
タイトル
タイトル Reciprocal regulatory mechanisms between the integrated stress response pathway and cyclin D1 in the mitochondrial stress response
言語 en
作成者 Hirao, Wataru

× Hirao, Wataru

en Hirao, Wataru

Department of Stress Response Science, Biomedical Research Center, Hirosaki University Graduate School of Medicine,Department of Glycobiology, Hirosaki University Graduate School of Medicine

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Mimura, Junsei

× Mimura, Junsei

en Mimura, Junsei

Department of Stress Response Science, Biomedical Research Center, Hirosaki University Graduate School of Medicine

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Kasai, Shuya

× Kasai, Shuya

en Kasai, Shuya

Department of Stress Response Science, Biomedical Research Center, Hirosaki University Graduate School of Medicine

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Itoh, Ken

× Itoh, Ken

en Itoh, Ken

Department of Stress Response Science, Biomedical Research Center, Hirosaki University Graduate School of Medicine

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アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
内容記述
内容記述タイプ Abstract
内容記述 Mitochondria are essential organelles that orchestrate a wide array of cellular processes, including energy production and apoptosis. Perturbations arising from both exogenous and endogenous stressors can compromise mitochondrial function, contributing to the pathogenesis of numerous human diseases and the aging process. Despite their critical roles, the regulatory mechanisms governing mitochondrial stress responses and their functional consequences remain poorly understood.  In the present study, we demonstrate that oligomycin-induced mitochondrial stress elicits downregulation of cyclin D1 (cycD1) and cell cycle arrest through activation of the integrated stress response (ISR) pathway in HEK293 cells. Moreover, we show that knockdown of cycD1 potentiates ISR activity in HeLa cells. Collectively, these findings uncover a previously unrecognized reciprocal crosstalk between cycD1 and the ISR pathway in the context of mitochondrial stress response.
言語 en
出版者
出版者 弘前大学大学院医学研究科
言語 ja
出版者
出版者 Hirosaki University Graduate School of Medicine
言語 en
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
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 NCID
収録物識別子 AN00211444
収録物識別子
収録物識別子タイプ PISSN
収録物識別子 0439-1721
収録物識別子
収録物識別子タイプ EISSN
収録物識別子 2434-4656
書誌情報 ja : 弘前医学
en : Hirosaki Medical Journal

巻 76, 号 1-4, p. 94-105, 発行日 2026-03-10
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