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  1. 010 学術雑誌論文
  2. 飯田, 香穂里 / IIDA, Kaori

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/3287
a5daee4d-0456-44f9-afc0-878be020ed27
名前 / ファイル ライセンス アクション
1471-2121-8-38.pdf 本文 (731.2 kB)
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Item type 学術雑誌論文 / Journal Article(1)
公開日 2012-12-12
タイトル
タイトル PERK eIF2 alpha kinase is required to regulate the viability of the exocrine pancreas in mice
タイトル
言語 en
タイトル PERK eIF2 alpha kinase is required to regulate the viability of the exocrine pancreas in mice
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 IIDA, Kaori

× IIDA, Kaori

WEKO 374

IIDA, Kaori

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LI, Yulin

× LI, Yulin

WEKO 720

LI, Yulin

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MCGRATH, Barbara C

× MCGRATH, Barbara C

WEKO 721

MCGRATH, Barbara C

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FRANK, Ami

× FRANK, Ami

WEKO 722

FRANK, Ami

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CAVENER, Douglas R

× CAVENER, Douglas R

WEKO 723

CAVENER, Douglas R

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著者別名 飯田, 香穂里

× 飯田, 香穂里

WEKO 373
NRID 1000010589667
e-Rad 10589667

飯田, 香穂里

Search repository
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.
書誌情報 BMC Cell Biology
en : BMC Cell Biology

巻 8, 発行日 2007-08-29
出版者
出版者 BioMed Central
ISSN
収録物識別子タイプ ISSN
収録物識別子 14712121
PubMed番号
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.
関連サイト
識別子タイプ URI
関連識別子 http://www.biomedcentral.com/about/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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