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  1. 原著論文

Upregulation of NRF2 through autophagy/ERK 1/2 ameliorates ionizing radiation induced cell death of human osteosarcoma U-2 OS

https://repo.qst.go.jp/records/47722
https://repo.qst.go.jp/records/47722
a40e9c75-6674-4de0-ac1e-afaa98b10dfc
Item type 学術雑誌論文 / Journal Article(1)
公開日 2017-04-19
タイトル
タイトル Upregulation of NRF2 through autophagy/ERK 1/2 ameliorates ionizing radiation induced cell death of human osteosarcoma U-2 OS
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
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Chen, Ni

× Chen, Ni

WEKO 478833

Chen, Ni

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Zhang, Rui

× Zhang, Rui

WEKO 478834

Zhang, Rui

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Konishi, Teruaki

× Konishi, Teruaki

WEKO 478835

Konishi, Teruaki

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Wang, Jun

× Wang, Jun

WEKO 478836

Wang, Jun

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小西 輝昭

× 小西 輝昭

WEKO 478837

en 小西 輝昭

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抄録
内容記述タイプ Abstract
内容記述 The antioxidative response mediated by transcription factor NRF2 is thought to be a pivotal cellular defense system against various extrinsic stresses. It has been reported that activation of the NRF2 pathway confers cells with resistance to ionizing radiation-induced damage. However, the underlying mechanism remains largely unknown. In the current research, it was found that α-particle radiation has the ability to stimulate NRF2 expression in human osteosarcoma U-2 OS cells. Knockdown of cellular NRF2 level by shRNA-mediated gene silencing decreased the survival rate, increased the micronucleus formation rate and apoptosis rate in irradiated cells. Consistently, knockdown of NRF2 resulted in decreased expression of p65 and Bcl-2, and increased expression of p53 and Bax. Besides, it was observed that increased expression of NRF2 was partially dependent on radiation induced phosphorylation of ERK 1/2. Further results showed that radiation promoted autophagy flux which leads to the enhanced phosphorylation of ERK 1/2, as evidenced by the resultls that knockdown of ATG5 (Autophagy protein 5) gene by shRNA suppressed both radiation induced ERK 1/2 phosphorylation and NRF2 upregulation. Based on these results, it is proposed that attenuation of NRF2 antioxidative pathway can sensitize U-2 OS cells to radiation, where NRF2 antioxidative response is regulated by autophagy mediated activation of ERK 1/2 kinases.
書誌情報 Mutation Research/Genetic Toxicology and Environmental Mutagenesis

巻 813, p. 10-17, 発行日 2017-01
出版者
出版者 Elsevier
ISSN
収録物識別子タイプ ISSN
収録物識別子 1383-5718
DOI
識別子タイプ DOI
関連識別子 10.1016/j.mrgentox.2016.11.006
関連サイト
識別子タイプ URI
関連識別子 http://www.sciencedirect.com/science/article/pii/S1383571816300742
関連名称 http://www.sciencedirect.com/science/article/pii/S1383571816300742
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