The full-length isoform of the mouse pleckstrin homology domain-interacting protein (PHIP) is required for postnatal growth |
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Authors: | Shuai Li Chunchun Han Shrivatsav Pattabiraman Sarah L. Giesy John C. Schimenti Qiaoming Long |
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Affiliation: | a Department of Animal Science, College of Agricultural and Life Sciences, Cornell University, Tower Road, Ithaca, NY 14850, United States b Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14850, United States |
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Abstract: | PHIP was isolated as an insulin receptor substrate 1 (IRS-1) interacting protein. To date, the physiological roles of PHIP remain unknown. Here we show that mice lacking PHIP1, the full-length isoform of PHIP, are born at normal size but suffer a 40% growth deficit by weaning. PHIP1 mutant mice develop hypoglycemia and have an average lifespan of 4-5 weeks. PHIP1-deficient mouse embryonic fibroblasts (MEFs) grow markedly slower than wild-type MEFs, but exhibit normal AKT phosphorylation and an increased cell proliferation in response to IGF-1 treatment. Together these results suggest that PHIP1 regulates postnatal growth in an IGF-1/AKT pathway-independent manner. |
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Keywords: | Insulin substrate IGF-1 signaling Postnatal growth Bromodomain Gene expression |
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