Separate pathways for p53 induction by ionizing radiation and N-(phosphonoacetyl)-L-aspartate.

Published

Journal Article

The tumor suppressor gene product, p53, appears to be a significant participant in signaling pathways that mediate cellular responses to cytotoxic stresses. In particular, p53 appears to be a critical determinant of whether the cell lives or dies and how it progresses through the cell cycle after the cytotoxic exposure. Many of the molecular details for these signaling pathways remain to be elucidated, and whether all cytotoxic signals utilize the same pathway to increase p53 expression is not clear. Here, we demonstrate the existence of cell types in which the induction of p53 and associated G1 arrest by the antimetabolite, N-(phosphonoacetyl)-L-aspartate (PALA), is defective, whereas p53 induction and G1 arrest induced by ionizing radiation are intact. These observations demonstrate the existence of genetic defects that can alter p53 induction and associated cellular outcomes after some, but not all, cytotoxic insults and suggest distinct pathways of p53 induction by PALA and ionizing radiation.

Full Text

Duke Authors

Cited Authors

  • Chen, CY; Hall, I; Lansing, TJ; Gilmer, TM; Tlsty, TD; Kastan, MB

Published Date

  • August 15, 1996

Published In

Volume / Issue

  • 56 / 16

Start / End Page

  • 3659 - 3662

PubMed ID

  • 8706003

Pubmed Central ID

  • 8706003

International Standard Serial Number (ISSN)

  • 0008-5472

Language

  • eng

Conference Location

  • United States