title: The insulin-like growth factor I receptor as a physiologically relevant target of p53 in apoptosis caused by interleukin-3 withdrawal.
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.
authors.affiliation: Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
authors.forename: M
authors.initials: M
authors.lastname: Prisco
authors.forename: A
authors.initials: A
authors.lastname: Hongo
authors.forename: M G
authors.initials: MG
authors.lastname: Rizzo
authors.forename: A
authors.initials: A
authors.lastname: Sacchi
authors.forename: R
authors.initials: R
authors.lastname: Baserga
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002460:Cell Line; D003587:Cytomegalovirus / Q000235:genetics; D006412:Hematopoietic Stem Cells; D006801:Humans; D007377:Interleukin-3 / Q000502:physiology*; D051379:Mice; D009154:Mutation; D011401:Promoter Regions, Genetic; D051381:Rats; D017526:Receptor, IGF Type 1 / Q000235:genetics / Q000502:physiology*; D013696:Temperature; D016159:Tumor Suppressor Protein p53 / Q000737:chemistry / Q000235:genetics / Q000502:physiology*
chemical_list: D007377:Interleukin-3; D016159:Tumor Suppressor Protein p53; D017526:Receptor, IGF Type 1