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J Biol Chem, Vol. 274, Issue 44, 31179-31184, October 29, 1999
From the Section on Molecular and Cellular Physiology, CEB/NIDDK,
National Institutes of Health, Bethesda, Maryland 20892-1758
The insulin receptor substrates (IRSs)-1-4 play
important roles in signal transduction emanating from the insulin and
insulin-like growth factor (IGF)-I receptors. IRS-4 is the most
recently characterized member, which has been found primarily in human
cells and tissues. It interacts with SH2-containing proteins such as
phosphatidylinositol 3'-kinase (PI3K), Grb2, Crk-II, and CrkL. In this
study, we transfected IRS-4 in mouse NIH-3T3 cells that overexpress
IGF-I receptors. Clones expressing IRS-4 showed enhanced cellular
proliferation when cells were cultured in 1% fetal bovine serum
without added IGF-I. Addition of IGF-I enhanced cellular proliferation
in cells overexpressing the IGF-I receptor alone but had an even
greater proliferative effect in cells overexpressing both the IGF-I
receptors and IRS-4. When etoposide and methylmethane sulfonate (MMS),
both DNA damaging agents, were added to the cells, they uniformly
induced cell cycle arrest. Fluorescence-activated cell sorter analysis demonstrated that the arrest of the cell cycle occurred at the G1 checkpoint, and furthermore no significant degree
of apoptosis was demonstrated with the use of either agent. In cells,
overexpressing IGF-I receptors alone, IGF-I addition enhanced cellular
proliferation, even in the presence of etoposide and MMS. In cells
overexpressing IGF-I receptors and IRS-4, the effect of IGF-I in
overcoming the cell cycle arrest was even more pronounced. These
results suggest that IRS-4 is implicated in the IGF-I receptor
mitogenic signaling pathway.
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