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

Marco Frisco, Atsushi Hongo, Maria Giulia Rizzo, Ada Sacchi, Renato Baserga

Research output: Contribution to journalArticle

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 1 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 dries not occur. These findings show that, in 32Dtsp53 cells, the IGF-IR is a physiologically relevant target of p53 in the process of apoptosis.

Original languageEnglish
Pages (from-to)1084-1092
Number of pages9
JournalMolecular and Cellular Biology
Volume17
Issue number3
Publication statusPublished - Mar 1997

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cell Biology

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