IGF-1 activates p21 to inhibit UV-induced cell death. Academic Article uri icon

Overview

abstract

  • The insulin-like growth factor-1 (IGF-1) and its downstream effector Akt have been documented as survival factors in response to a variety of stress signals. In this study, we show that IGF-1 activates p21 protein expression in a p53-dependent manner. Inhibition of PI-3 kinase or ectopic expression of a dominant-negative Akt blocks the effect of IGF-1 on the upregulation of p21 expression. In addition, IGF-1 prevents the UV irradiation-mediated suppression of p21 and MDM2 expression. Furthermore, p21 is important for IGF-1-mediated cell survival upon UV irradiation. Taken together, these data indicate that IGF-1 may activate p21 in executing its survival function upon genotoxic insults.

publication date

  • March 20, 2003

Research

keywords

  • Apoptosis
  • Cyclins
  • Insulin-Like Growth Factor I
  • Nuclear Proteins
  • Protein Serine-Threonine Kinases
  • Protein-Serine-Threonine Kinases
  • Ultraviolet Rays

Identity

Scopus Document Identifier

  • 0037457059

PubMed ID

  • 12642873

Additional Document Info

volume

  • 22

issue

  • 11