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Double-stranded RNA-activated protein kinase (PKR) fused to green fluorescent protein induces apoptosis of human embryonic kidney cells: Possible role in the Fas signaling pathway
http://hdl.handle.net/2297/14558
http://hdl.handle.net/2297/14558a81c2c15-0c88-4875-bb9b-67c6cfb9bdc8
名前 / ファイル | ライセンス | アクション |
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PH-PR-NAKANISHI-Y-391.pdf (6.3 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-04 | |||||
タイトル | ||||||
タイトル | Double-stranded RNA-activated protein kinase (PKR) fused to green fluorescent protein induces apoptosis of human embryonic kidney cells: Possible role in the Fas signaling pathway | |||||
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 |
Takizawa, Takenori
× Takizawa, Takenori× Tatematsu, Chizuru× Nakanishi, Yoshinobu |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学医薬保健研究域薬学系 | |||||
書誌情報 |
Journal of Biochemistry 巻 125, 号 2, p. 391-398, 発行日 1999-01-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0021-924X | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00694073 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1093/oxfordjournals.jbchem.a022299 | |||||
出版者 | ||||||
出版者 | 日本生化学会 = Japanese Biochemical Society | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | PKR is an interferon-inducible, double-stranded (ds) RNA-activated serine/threonine protein kinase, and has been shown to play roles in viral pathogenesis, cell growth and apoptosis. We expressed PKR as a fusion protein with enhanced jellyfish green fluorescence protein (EGFP) in human embryonic kidney 293 cells to visualize the effect of PKR transfection. The EGFP-fusion construct with wild-type PKR showed both auto- and substrate-phosphorylation activities independent of dsRNA, indicating EGFP-PKR is constitutively active. The EGFP-construct with a mutant PKR with the first RNA binding domain deleted still possessed kinase activities. On the other hand, the EGFP-fusion with a catalytically inactive mutant of PKR with the substitution of K at 296 with R, which has been shown to have tumorigenic properties, did not possess kinase activities. Transfection of the constitutive active forms of EGFP-PKR constructs induced apoptosis in 293 cells without dsRNA, whereas the EGFP-fusion with the catalytically inactive mutant did not cause apoptosis but rather protected cells from Fas-induced cell death. In addition, Fas-stimulation increased endogenous PKR activities. These results constitute evidence that PKR is sufficient to induce apoptosis, and plays a role in Fas-mediated apoptosis. | |||||
権利 | ||||||
権利情報 | Copyright © 1999 Japanese Biochemical Society | |||||
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 | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | http://jb.oxfordjournals.org/cgi/content/abstract/125/2/391 |