@article{oai:ir.soken.ac.jp:00003289,
 author = {飯田, 香穂里 and LI, Yulin and IIDA, Kaori and O’NEIL, Jeff and ZHANG, Peichuan and LI, Sheng’ai and FRANK, Ami and GABAI, Aryn and ZAMBITO, Frank and LIANG, Shun-Hsin and ROSEN, Clifford J and CAVENER, Douglas R},
 issue = {8},
 journal = {Endocrinology, Endocrinology},
 month = {Apr},
 note = {application/pdf, 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.},
 pages = {3505--3513},
 title = {PERK eIF2α kinase regulates neonatal growth by controlling the expression of circulating insulin-like growth factor-I derived from the liver},
 volume = {144},
 year = {2003}
}