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Reversion-inducing cysteine-rich protein with Kazal motifs interferes with epidermal growth factor receptor signaling
https://doi.org/10.24517/00027532
https://doi.org/10.24517/00027532ed97c17d-5a16-430a-9c5d-76143455f857
| 名前 / ファイル | ライセンス | アクション |
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CA-PR-TAKAHASI-C-737.pdf (760.3 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||
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| 公開日 | 2017-10-05 | |||||||||
| タイトル | ||||||||||
| タイトル | Reversion-inducing cysteine-rich protein with Kazal motifs interferes with epidermal growth factor receptor signaling | |||||||||
| 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 | |||||||||
| ID登録 | ||||||||||
| ID登録 | 10.24517/00027532 | |||||||||
| ID登録タイプ | JaLC | |||||||||
| 著者 |
Kitajima, Shunsuke
× Kitajima, Shunsuke× Miki, T.× Takegami, Yujiro× Kido, Y.× Noda, M.× Hara, Eiji× Shamma, Awad× Takahashi, Chiaki |
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| 著者別表示 |
北嶋, 俊輔
× 北嶋, 俊輔
× 高橋, 智聡
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| 提供者所属 | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | 金沢大学がん研究所 | |||||||||
| 書誌情報 |
Oncogene 巻 30, 号 6, p. 737-750, 発行日 2011-02-10 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | ISSN | |||||||||
| 収録物識別子 | 0950-9232 | |||||||||
| NCID | ||||||||||
| 収録物識別子タイプ | NCID | |||||||||
| 収録物識別子 | AA10687380 | |||||||||
| DOI | ||||||||||
| 関連タイプ | isVersionOf | |||||||||
| 識別子タイプ | DOI | |||||||||
| 関連識別子 | 10.1038/onc.2010.448 | |||||||||
| 出版者 | ||||||||||
| 出版者 | Nature Publishing Group | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | The reversion-inducing cysteine-rich protein with Kazal motifs (RECK) gene had been isolated as an antagonist to RAS signaling; however, the mechanism of its action is not clear. In this study, the effect of loss of RECK function was assessed in various ways and cell systems. Successive cell cultivation of mouse embryonic fibroblasts (MEFs) according to 3T3 protocol revealed that the germline knockout of RECK confers accelerated cell proliferation and early escape from cellular senescence associated with downregulation of p19 Arf, Trp53 and p21Cdkn1a. In contrast, short hairpin RNA-mediated depletion of RECK induced irreversible growth arrest along with several features of the Arf, Trp53 and Cdkn1a-dependent cellular senescence. Within 2 days of RECK depletion, we observed a transient increase in protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) phosphorylation associated with an upregulated expression of cyclin D1, p19Arf, Trp53, p21Cdkn1a and Sprouty 2. On further cultivation, RAS, AKT and ERK activities were then downregulated to a level lower than control, indicating that RECK depletion leads to a negative feedback to RAS signaling and subsequent cellular senescence. In addition, we observed that epidermal growth factor receptor (EGFR) activity was transiently upregulated by RECK depletion in MEFs, and continuously downregulated by RECK overexpression in colon cancer cells. These findings indicate that RECK is a novel modulator of EGFR signaling. © 2011 Macmillan Publishers Limited All rights reserved. | |||||||||
| 著者版フラグ | ||||||||||
| 出版タイプ | AM | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||
