Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2048470 | FEBS Letters | 2010 | 7 Pages |
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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Authors
Shuai Li, Adam B. Francisco, Chunchun Han, Shrivatsav Pattabiraman, Monica R. Foote, Sarah L. Giesy, Chong Wang, John C. Schimenti, Yves R. Boisclair, Qiaoming Long,