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  1. 原著論文

Ku80 attentuates cytotoxicity induced by green fluorescent protein transduction independently of non-homologous end joining.

https://repo.qst.go.jp/records/46558
https://repo.qst.go.jp/records/46558
42111268-9513-4118-9750-9a1bf0935db0
Item type 学術雑誌論文 / Journal Article(1)
公開日 2013-06-07
タイトル
タイトル Ku80 attentuates cytotoxicity induced by green fluorescent protein transduction independently of non-homologous end joining.
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 Koike, Manabu

× Koike, Manabu

WEKO 464026

Koike, Manabu

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Yutoku, Yasutomo

× Yutoku, Yasutomo

WEKO 464027

Yutoku, Yasutomo

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Koike, Aki

× Koike, Aki

WEKO 464028

Koike, Aki

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小池 学

× 小池 学

WEKO 464029

en 小池 学

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湯徳 靖友

× 湯徳 靖友

WEKO 464030

en 湯徳 靖友

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小池 亜紀

× 小池 亜紀

WEKO 464031

en 小池 亜紀

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抄録
内容記述タイプ Abstract
内容記述 The green fluorescent protein (GFP) is the most commonly used reporter protein for monitoring gene expression and protein localization in a variety of living and fixed cells, including not only prokaryotes, but also eukaryotes, e.g., yeasts, mammals, plants and fish. In general, it is thought that GFP is nontoxic to cells, although there are some reports on the side effect of GFP. Further, details of the molecular mechanism concerning the side effect of GFP remain unclear. Here we show that Ku80, but not XRCC4, plays an important role in the mechanism of the resistance to cytotoxicity induced by enhanced GFP (EGFP). EGFP inhibited both cell proliferation and colony formation, and induced cell death in Ku80-deficient hamster cells, i.e., xrs-6 cells. In addition, Ku80 attenuated EGFP-induced cytotoxicity in the xrs-6 cells. No EGFP-induced cytotoxicity was observed in the NHEJ core protein XRCC4-deficient hamster cells, i.e., XR-1 cells. Furthermore, EGFP markedly enhanced X-ray-induced cytotoxicity in the xrs-6 cells. These results suggest that Ku80 plays a key role in the novel NHEJ-independent defense mechanism against EGFP-induced cytotoxicity. Caution should be taken in considering of the potential influence by the stress response mechanism, namely, the Ku80-dependent elimination mechanism of EGFP-induced cytotoxicity, being activated, even when using EGFP-expressing cells in which Ku80 functions normally.
書誌情報 FEBS Open Bio (Online Only URL:http://www.sciencedirect.com/science/journal/22115463)

巻 3, p. 46-50, 発行日 2012-12
ISSN
収録物識別子タイプ ISSN
収録物識別子 2211-5463
関連サイト
識別子タイプ URI
関連識別子 http://www.sciencedirect.com/science/journal/22115463
関連名称 http://www.sciencedirect.com/science/journal/22115463
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