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Review Article A Novel Regulatory Mechanism of Apoptosis by Calreticulin, a Molecular Chaperone in the Endoplasmic Reticulum
http://hdl.handle.net/10069/16250
http://hdl.handle.net/10069/16250f92fb00c-b410-48c5-ae82-fe034628ef09
名前 / ファイル | ライセンス | アクション |
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acta48_03_01_t.pdf (1.1 MB)
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Item type | 紀要論文 / Departmental Bulletin Paper(1) | |||||
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公開日 | 2008-03-13 | |||||
タイトル | ||||||
タイトル | Review Article A Novel Regulatory Mechanism of Apoptosis by Calreticulin, a Molecular Chaperone in the Endoplasmic Reticulum | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | calreticulin | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | endoplasmic reticulum | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | molecular chaperone | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | calcium | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | akt/protein kinase B | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | apoptosis | |||||
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 | departmental bulletin paper | |||||
著者 |
Ihara, Yoshito
× Ihara, Yoshito |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Calreticulin (CRT) is a Ca"--binding lectin-like molecular chaperone of the lumen of the endoplasmic reticulum. Recently, CRT has been revealed to be a multi-functional molecule related with glycoprotein maturation and chaperone function, Ca" homeostasis, cell adhesion, cell signaling, transcriptional regulation, and nuclear transporting mechanisms. CRT is also essential for cardiac and neural development in mice, suggesting an importance in the regulation of cell survival and death during development. To examine the role of CRT in cardiac differentiation, we established CRT-overexpressiog myocardiac H9c2 cells, and investigated the effect of the overexpression on cardiac differentiation in vitro. We found that the cells transfected with the CRT gene were highly susceptible to apoptosis compared with controls. In the gene-transfected cells, Akt/ protein kinase B signaling was significantly suppressed during the differentiation. Furthermore, PP2A, a Ser/Thr protein phosphatase, was significantly upregulated implying a suppression of Akt signaling due to dephosphorylation of Alit by the upregulated PP2A via the regulation of Ca` homeostasis. Thus, overexpression of CRT promotes differentiation- dependent apoptosis in H9c2 cells by suppressing the Akt signaling pathway. Our findings demonstrate a novel mechanism in which cytoplasmic Akt signaling is modulated to cause apoptosis by a resident protein of the endoplasmic reticulum, CRT. | |||||
書誌情報 |
Acta medica Nagasakiensia 巻 48, 号 3-4, p. 85-92, 発行日 2003-12-24 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 00016055 | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00508430 | |||||
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 | |||||
sortkey | ||||||
P00085-P00092 | ||||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | Acta medica Nagasakiensia. 2003, 48(3-4), p.85-92 |