The insulin-like growth factor I receptor as a physiologically relevant target of p53 in apoptosis caused by interleukin-3 withdrawal - PubMed (original) (raw)

The insulin-like growth factor I receptor as a physiologically relevant target of p53 in apoptosis caused by interleukin-3 withdrawal

M Prisco et al. Mol Cell Biol. 1997 Mar.

Abstract

The wild-type p53 protein is known to modulate apoptosis induced in 32D murine hemopoietic cells by interleukin-3 withdrawal. In 32D cells and in 32D cells constitutively expressing a temperature-sensitive mutant of p53 (32Dtsp53), overexpression of a wild-type (but not a mutant) insulin-like growth factor I receptor (IGF-IR) protects these cells from apoptosis. A tsp53 in its wild-type conformation causes a decrease in the levels of IGF-IRs, and this decrease is accompanied by increased sensitivity of these cells to apoptosis. However, when the expression of the IGF-IR cDNA is regulated by a viral promoter, IGF-IR levels are not decreased by a wild-type p53, and apoptosis does not occur. These findings show that, in 32Dtsp53 cells, the IGF-IR is a physiologically relevant target of p53 in the process of apoptosis.

PubMed Disclaimer

References

1. Proc Natl Acad Sci U S A. 1979 Mar;76(3):1279-83 - PubMed
1. Mol Cell Biol. 1994 Jul;14(7):4427-34 - PubMed
1. Proc Natl Acad Sci U S A. 1985 May;82(10):3169-72 - PubMed
1. EMBO J. 1986 Oct;5(10):2503-12 - PubMed
1. Gene. 1988;62(1):121-6 - PubMed

The insulin-like growth factor I receptor as a physiologically relevant target of p53 in apoptosis caused by interleukin-3 withdrawal - PubMed (original) (raw)