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

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/3289
294bf56b-c0b3-48c9-93e8-43e917abc595
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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 eIF2α kinase regulates neonatal growth by controlling the expression of circulating insulin-like growth factor-I derived from the liver
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
言語 en
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

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LI, Yulin

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IIDA, Kaori

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IIDA, Kaori

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O’NEIL, Jeff

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O’NEIL, Jeff

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ZHANG, Peichuan

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ZHANG, Peichuan

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LI, Sheng’ai

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LI, Sheng’ai

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FRANK, Ami

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FRANK, Ami

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GABAI, Aryn

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GABAI, Aryn

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ZAMBITO, Frank

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ZAMBITO, Frank

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LIANG, Shun-Hsin

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LIANG, Shun-Hsin

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ROSEN, Clifford J

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ROSEN, Clifford J

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CAVENER, Douglas R

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CAVENER, Douglas R

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著者別名 飯田, 香穂里

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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
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
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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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