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PERK eIF2α kinase regulates neonatal growth by controlling the expression of circulating insulin-like growth factor-I derived from the liver
https://ir.soken.ac.jp/records/3289
https://ir.soken.ac.jp/records/3289294bf56b-c0b3-48c9-93e8-43e917abc595
名前 / ファイル | ライセンス | アクション |
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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 | |||||
タイトル | ||||||
タイトル | PERK eIF2α kinase regulates neonatal growth by controlling the expression of circulating insulin-like growth factor-I derived from the liver | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | PERK eIF2α kinase regulates neonatal growth by controlling the expression of circulating insulin-like growth factor-I derived from the liver | |||||
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 |
LI, Yulin
× LI, Yulin× IIDA, Kaori× O’NEIL, Jeff× ZHANG, Peichuan× LI, Sheng’ai× FRANK, Ami× GABAI, Aryn× ZAMBITO, Frank× LIANG, Shun-Hsin× ROSEN, Clifford J× 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 | Humans afflicted with the Wolcott-Rallison syndrome and mice deficient for PERK (pancreatic endoplasmic reticulum eIF2α kinase) show severe postnatal growth retardation. In mice, growth retardation in Perk−/− mutants is manifested within the first few days of neonatal development. Growth parameters of Perk−/− mice, including comparison of body weight to length and organ weights, are consistent with proportional dwarfism. Tibia growth plates exhibited a reduction in proliferative and hypertrophic chondrocytes underlying the longitudinal growth retardation. Neonatal Perk−/− deficient mice show a 75% reduction in liver IGF-I mRNA and serum IGF-I within the first week, whereas the expression of IGF-I mRNA in most other tissues is normal. Injections of IGF-I partially reversed the growth retardation of the Perk−/− mice, whereas GH had no effect. Transgenic rescue of PERK activity in the insulin- secreting β-cells of the Perk−/− mice reversed the juvenile but not the neonatal growth retardation. We provide evidence that circulating IGF-I is derived from neonatal liver but is independent of GH at this stage. We propose that PERK is required to regulate the expression of IGF-I in the liver during the neonatal period, when IGF-I expression is GH-independent, and that the lack of this regulation results in severe neonatal growth retardation. | |||||
書誌情報 |
Endocrinology en : Endocrinology 巻 144, 号 8, p. 3505-3513, 発行日 2003-04-11 |
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出版者 | ||||||
出版者 | The Endocrine Society | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 00137227 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1210/en.2003-0236 | |||||
関連名称 | 10.1210/en.2003-0236 | |||||
権利 | ||||||
権利情報 | © 2003 by The Endocrine Society | |||||
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 |