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  1. 0800 先端科学技術推進機構(ORDIST)
  2. 先端科学技術シンポジウム講演集
  3. 第11回

神経系小胞体ストレスと誘導型アポトーシスのニコチンとニューロトロフィンによる防御機構

http://hdl.handle.net/10112/2210
http://hdl.handle.net/10112/2210
5314eed6-02db-48f3-8fe9-af624533e4c3
名前 / ファイル ライセンス アクション
KU-0800-20070110-01.pdf KU-0800-20070110-01.pdf (869.4 kB)
Item type 会議発表論文 / Conference Paper(1)
公開日 2010-07-16
タイトル
タイトル 神経系小胞体ストレスと誘導型アポトーシスのニコチンとニューロトロフィンによる防御機構
言語 ja
言語
言語 jpn
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_5794
資源タイプ conference paper
著者 池内, 俊彦

× 池内, 俊彦

WEKO 27745
e-Rad 20093362

ja 池内, 俊彦

en Ikeuchi, Toshihiko

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下家, 浩二

× 下家, 浩二

WEKO 6729
e-Rad 10351496

ja 下家, 浩二

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著者別名
識別子Scheme WEKO
識別子 6731
姓名 Shimoke, Koji
概要
内容記述タイプ Other
内容記述 Neuronal degenerative diseases including Alzheimer's, Parkinson's and polyglutamine diseases are considered to involve endoplasmic reticulum (ER) stress, which leads to ER stress-mediated apoptosis of some neurons. In the process of these diseases, it has been reported that unfolded proteins are accumulated in the ER and this step is critical for progression of neuronal apoptosis through the caspase cascade involving an ER stress-specific caspase, caspase-12. During ER stress, chaperone proteins including glucose-regulated protein 78 (GRP78) are expressed to fold these unfolded proteins as an unfolded protein response (UPR). In cultured cells, ER stress can be induced by tunicamycin (Tm) or thapsigargin (Tg).
We report that nerve growth factor (NGF), a well-known member of the neurotrophin family, suppressed Tm-, Tg- and 2-deoxy-glucose (2DG)-induced ER stress-mediated apoptosis in PC12 cells as a model neuron. NGF prevented the progression of ER stress-induced apoptosis by the suppression of activation of caspase-12 via the PI3-kinase-Akt signaling pathway. NGF up-regulated the ER stress-stimulated expression of GRP78, but this up-regulation of GRP78 by NGF did not contribute to the protective effect ofNGF on ER stress-induced apoptosis.
We found that nicotine protected against Tm-induced ER stress-mediated apoptosis but not Tg-induced ER stress-mediated apoptosis in PC12 cells. We also found that the expression of GRP78 was suppressed by nicotine in Tm-treated PC12 cells. Interestingly, the expression of GRP78 was not changed by nicotine in Tg-treated cells. Moreover, nicotine reduced the activation of caspase-12 in Tm-treated cells, but not in Tg-treated cells. These results suggest that nicotine prevents Tm-induced ER stress-mediated apoptosis by attenuating Tm-induced ER stress itself, probably by the clearance of accumulated unfolded proteins from the ER.
内容記述
内容記述タイプ Other
内容記述 This work was supported in part by grants-in-aid for scientific research from MEXT, HAITEKU (2002-2006) from MEXT and a research grant from the Smoking Research Foundation.
書誌情報 第11回関西大学先端科学技術シンポジウム講演集

p. 109-116, 発行日 2007-01-10
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
出版者
出版者 関西大学先端科学技術推進機構
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Cite as

池内, 俊彦, 下家, 浩二, 2007, 神経系小胞体ストレスと誘導型アポトーシスのニコチンとニューロトロフィンによる防御機構: 関西大学先端科学技術推進機構, 109–116 p.

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