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

被引:135
作者
Prisco, M
Hongo, A
Rizzo, MG
Sacchi, A
Baserga, R
机构
[1] THOMAS JEFFERSON UNIV,KIMMEL CANC CTR,PHILADELPHIA,PA 19107
[2] IST REGINA ELENA,LAB ONCOGENSESI MOL,I-00161 ROME,ITALY
关键词
D O I
10.1128/MCB.17.3.1084
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:1084 / 1092
页数:9
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