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PMID: 9032235 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

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

Molecular and cellular biology ·Vol. 17 ·No. 3 ·1997-03-00 ·Pages 1084-92

Prisco M, Hongo A, Rizzo MG, Sacchi A, Baserga R

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.

MeSH Terms
Animals Apoptosis/physiology Cell Line Cytomegalovirus/genetics Hematopoietic Stem Cells Humans Interleukin-3/physiology Mice Mutation Promoter Regions, Genetic Rats Receptor, IGF Type 1/genetics,physiology Temperature Tumor Suppressor Protein p53/chemistry,genetics,physiology
Chemicals
Interleukin-3 Tumor Suppressor Protein p53 Receptor, IGF Type 1
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Prisco M
Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Hongo A
Rizzo M G
Sacchi A
Baserga R
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Article Info
Journal
Molecular and cellular biology
Abbr.
Mol Cell Biol
ISSN
0270-7306
DOI
10.1128/MCB.17.3.1084
Published
1997-03-00
Pages
1084-92
Language
English
Region
United States
NLM ID
8109087
PMCID
PMC231833
Subset
IM
Grants
NIGMS NIH HHS · GM 33694 · United States
External Links
PubMed source DOI: 10.1128/MCB.17.3.1084 PMC Full Text View journal details
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