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PERK eIF2 alpha kinase is required to regulate the viability of the exocrine pancreas in mice
https://ir.soken.ac.jp/records/3287
https://ir.soken.ac.jp/records/3287a5daee4d-0456-44f9-afc0-878be020ed27
名前 / ファイル | ライセンス | アクション |
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本文 (731.2 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2012-12-12 | |||||
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タイトル | PERK eIF2 alpha kinase is required to regulate the viability of the exocrine pancreas in mice | |||||
タイトル | ||||||
タイトル | PERK eIF2 alpha kinase is required to regulate the viability of the exocrine pancreas in mice | |||||
言語 | en | |||||
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言語 | eng | |||||
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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 |
IIDA, Kaori
× IIDA, Kaori× LI, Yulin× MCGRATH, Barbara C× FRANK, Ami× CAVENER, Douglas R |
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著者別名 |
飯田, 香穂里
× 飯田, 香穂里 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Background Deficiency of the PERK eIF2α kinase in humans and mice results in postnatal exocrine pancreatic atrophy as well as severe growth and metabolic anomalies in other organs and tissues. To determine if the exocrine pancreatic atrophy is due to a cell-autonomous defect, the Perk gene was specifically ablated in acinar cells of the exocrine pancreas in mice. Results We show that expression of PERK in the acinar cells is required to maintain their viability but is not required for normal protein synthesis and secretion. Exocrine pancreatic atrophy in PERK-deficient mice was previously attributed to uncontrolled ER-stress followed by apoptotic cell death based on studies in cultured fibroblasts. However, we have found no evidence for perturbations in the endoplasmic reticulum or ER-stress and show that acinar cells succumb to a non-apoptotic form of cell death, oncosis, which is associated with a pronounced inflammatory response and induction of the pancreatitis stress response genes. We also show that mice carrying a knockout mutation of PERK's downstream target, ATF4, exhibit pancreatic deficiency caused by developmental defects and that mice ablated for ATF4's transcriptional target CHOP have a normal exocrine pancreas. Conclusion We conclude that PERK modulates secretory capacity of the exocrine pancreas by regulating cell viability of acinar cells. |
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書誌情報 |
BMC Cell Biology en : BMC Cell Biology 巻 8, 発行日 2007-08-29 |
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出版者 | ||||||
出版者 | BioMed Central | |||||
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収録物識別子タイプ | ISSN | |||||
収録物識別子 | 14712121 | |||||
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関連タイプ | isIdenticalTo | |||||
識別子タイプ | PMID | |||||
関連識別子 | 17727724 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1186/1471-2121-8-38 | |||||
関連名称 | 10.1186/1471-2121-8-38 | |||||
権利 | ||||||
権利情報 | © 2007 Iida et al; licensee BioMed Central Ltd. | |||||
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識別子タイプ | URI | |||||
関連識別子 | http://www.biomedcentral.com/about/license | |||||
関連名称 | Copyright | |||||
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内容記述タイプ | Other | |||||
内容記述 | application/pdf | |||||
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出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |