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The full-length isoform of the mouse pleckstrin homology domain-interacting protein (PHIP) is required for postnatal growth.
- Source :
-
FEBS letters [FEBS Lett] 2010 Sep 24; Vol. 584 (18), pp. 4121-7. Date of Electronic Publication: 2010 Sep 04. - Publication Year :
- 2010
-
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.<br /> (Copyright © 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.)
- Subjects :
- Animals
Cell Proliferation
Female
Hypoglycemia genetics
Insulin-Like Growth Factor I metabolism
Intracellular Signaling Peptides and Proteins
Mice
Mice, Mutant Strains
Nerve Tissue Proteins genetics
Protein Isoforms genetics
Protein Isoforms metabolism
Proto-Oncogene Proteins c-akt metabolism
Failure to Thrive genetics
Nerve Tissue Proteins metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1873-3468
- Volume :
- 584
- Issue :
- 18
- Database :
- MEDLINE
- Journal :
- FEBS letters
- Publication Type :
- Academic Journal
- Accession number :
- 20816727
- Full Text :
- https://doi.org/10.1016/j.febslet.2010.08.042