| First Author | Li S | Year | 2010 |
| Journal | FEBS Lett | Volume | 584 |
| Issue | 18 | Pages | 4121-7 |
| PubMed ID | 20816727 | Mgi Jnum | J:164354 |
| Mgi Id | MGI:4833711 | Doi | 10.1016/j.febslet.2010.08.042 |
| Citation | Li S, et al. (2010) The full-length isoform of the mouse pleckstrin homology domain-interacting protein (PHIP) is required for postnatal growth. FEBS Lett 584(18):4121-7 |
| abstractText | 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. |
