The full-length isoform of the mouse pleckstrin homology domain-interacting protein (PHIP) is required for postnatal growth.

FEBS letters

PubMedID: 20816727

Li S, Francisco AB, Han C, Pattabiraman S, Foote MR, Giesy SL, Wang C, Schimenti JC, Boisclair YR, Long Q. The full-length isoform of the mouse pleckstrin homology domain-interacting protein (PHIP) is required for postnatal growth. FEBS Lett. 2010;584(18):4121-7.
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.