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  1. 010 学術雑誌論文
  2. 田辺, 秀之 / TANABE, Hideyuki

Periostin Associates with Notch1 Precursor to Maintain Notch1 Expression under a Stress Condition in Mouse Cells

https://ir.soken.ac.jp/records/3958
https://ir.soken.ac.jp/records/3958
52c199d4-692e-473d-a4a0-8e046a4ebd0f
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Item type 学術雑誌論文 / Journal Article(1)
公開日 2013-09-18
タイトル
タイトル Periostin Associates with Notch1 Precursor to Maintain Notch1 Expression under a Stress Condition in Mouse Cells
タイトル
タイトル Periostin Associates with Notch1 Precursor to Maintain Notch1 Expression under a Stress Condition in Mouse Cells
言語 en
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 TANABE, Hideyuki

× TANABE, Hideyuki

TANABE, Hideyuki

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TAKAYAMA, Issei

× TAKAYAMA, Issei

TAKAYAMA, Issei

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NISHIYAMA, Takashi

× NISHIYAMA, Takashi

NISHIYAMA, Takashi

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et, al.

× et, al.

et, al.

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抄録
内容記述タイプ Abstract
内容記述 Background
Matricellular proteins, including periostin, modulate cell-matrix interactions and cell functions by acting outside of cells.

Methods and Findings
In this study, however, we reported that periostin physically associates with the Notch1 precursor at its EGF repeats in the inside of cells. Moreover, by using the periodontal ligament of molar from periostin-deficient adult mice (Pn−/− molar PDL), which is a constitutively mechanically stressed tissue, we found that periostin maintained the site-1 cleaved 120-kDa transmembrane domain of Notch1 (N1™) level without regulating Notch1 mRNA expression. N1™ maintenance in vitro was also observed under such a stress condition as heat and H2O2 treatment in periostin overexpressed cells. Furthermore, we found that the expression of a downstream effector of Notch signaling, Bcl-xL was decreased in the Pn−/− molar PDL, and in the molar movement, cell death was enhanced in the pressure side of Pn−/− molar PDL.

Conclusion
These results suggest the possibility that periostin inhibits cell death through up-regulation of Bcl-xL expression by maintaining the Notch1 protein level under the stress condition, which is caused by its physical association with the Notch1 precursor.
書誌情報 PLoS ONE
en : PLoS ONE

巻 5, 号 8, p. e12234, 発行日 2010-08-18
出版者
出版者 Public Library of Science
ISSN
収録物識別子タイプ ISSN
収録物識別子 1932-6203
DOI
関連タイプ isIdenticalTo
識別子タイプ DOI
関連識別子 https://doi.org/10.1371/journal.pone.0012234
関連名称 10.1371/journal.pone.0012234
権利
権利情報 © 2010 Tanabe et al
関連サイト
識別子タイプ URI
関連識別子 http://www.plos.org/about/open-access/license/
関連名称 Copyright
フォーマット
内容記述タイプ Other
内容記述 application/pdf
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
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