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  1. 030 医学部 = School of Medicine
  2. 030 学術雑誌論文 = Articles in academic journal

FK506 reduces abnormal prion protein through the activation of autolysosomal degradation and prolongs survival in prion-infected mice

http://hdl.handle.net/10069/33945
http://hdl.handle.net/10069/33945
c7b63d43-3e18-40be-bbea-523a7dcecaf4
名前 / ファイル ライセンス アクション
Aupha9_1386.pdf Aupha9_1386.pdf (1.1 MB)
アイテムタイプ 学術雑誌論文 / Journal Article(1)
公開日 2013-11-07
タイトル
タイトル FK506 reduces abnormal prion protein through the activation of autolysosomal degradation and prolongs survival in prion-infected mice
言語
言語 eng
キーワード
主題Scheme Other
主題 Autophagy
キーワード
主題Scheme Other
主題 Degradation
キーワード
主題Scheme Other
主題 FK506
キーワード
主題Scheme Other
主題 Microglia; Prion
キーワード
主題Scheme Other
主題 Tacrolimus
キーワード
主題Scheme Other
主題 Therapy
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 Nakagaki, Takehiro

× Nakagaki, Takehiro

Nakagaki, Takehiro

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Satoh, Katsuya

× Satoh, Katsuya

Satoh, Katsuya

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Ishibashi, Daisuke

× Ishibashi, Daisuke

Ishibashi, Daisuke

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Fuse, Takayuki

× Fuse, Takayuki

Fuse, Takayuki

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Sano, Kazunori

× Sano, Kazunori

Sano, Kazunori

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Kamatari, Yuji O.

× Kamatari, Yuji O.

Kamatari, Yuji O.

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Kuwata, Kazuo

× Kuwata, Kazuo

Kuwata, Kazuo

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Shigematsu, Kazuto

× Shigematsu, Kazuto

Shigematsu, Kazuto

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Iwamaru, Yoshifumi

× Iwamaru, Yoshifumi

Iwamaru, Yoshifumi

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Takenouchi, Takato

× Takenouchi, Takato

Takenouchi, Takato

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Kitani, Hiroshi

× Kitani, Hiroshi

Kitani, Hiroshi

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Nishida, Noriyuki

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Nishida, Noriyuki

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Atarashi, Ryuichiro

× Atarashi, Ryuichiro

Atarashi, Ryuichiro

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抄録
内容記述タイプ Abstract
内容記述 Prion diseases are fatal neurodegenerative disorders and no effective treatment has been established to date. In this study, we evaluated the effect of FK506 (tacrolimus), a macrolide that is known to be a mild immunosuppressant, on prion infection, using cell culture and animal models. We found that FK506 markedly reduced the abnormal form of prion protein (PRNPSc) in the cell cultures (N2a58 and MG20) infected with Fukuoka-1 prion. The levels of autophagy-related molecules such as LC3-II , ATG12-ATG5 and ATG7 were significantly increased in the FK506-treated cells, and resulted in the increased formation of autolysosomes. Upregulation of the autophagy-related molecules was also seen in the brains of FK506-treated mice and the accumulation of PRNPSc was delayed. The survival periods in mice inoculated with Fukuoka-1 were significantly increased when FK506 was administered from day 20 post-inoculation. These findings provide evidence that FK506 could constitute a novel antiprion drug, capable of enhancing the degradation of PRNPSc in addition to attenuation of microgliosis and neuroprotection.
書誌情報 Autophagy

巻 9, 号 9, p. 1386-1394, 発行日 2013-09
出版者
出版者 Landes Bioscience
ISSN
収録物識別子タイプ ISSN
収録物識別子 15548627
DOI
関連タイプ isIdenticalTo
識別子タイプ DOI
関連識別子 10.4161/auto.25381
権利
権利情報 © 2013 Landes Bioscience.
権利
権利情報 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
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
引用
内容記述タイプ Other
内容記述 Autophagy, 9(9), pp.1386-1394; 2013
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