Interleukin 3-dependent survival by the Akt protein kinase

Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11345-50. doi: 10.1073/pnas.94.21.11345.

Abstract

Interleukin 3 (IL-3)-dependent survival of hematopoietic cells is known to rely on the activity of multiple signaling pathways, including a pathway leading to activation of phosphoinositide 3-kinase (PI 3-kinase), and protein kinase Akt is a direct target of PI 3-kinase. We find that Akt kinase activity is rapidly induced by the cytokine IL-3, suggesting a role for Akt in PI 3-kinase-dependent signaling in hematopoetic cells. Dominant-negative mutants of Akt specifically block Akt activation by IL-3 and interfere with IL-3-dependent proliferation. Overexpression of Akt or oncogenic v-akt protects 32D cells from apoptosis induced by IL-3 withdrawal. Apoptosis after IL-3 withdrawal is accelerated by expression of dominant-negative mutants of Akt, indicating that a functional Akt signaling pathway is necessary for cell survival mediated by the cytokine IL-3. Thus Akt appears to be an important mediator of anti-apoptotic signaling in this system.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Division
  • Cell Line
  • Cell Survival / drug effects
  • Cell Survival / physiology*
  • Culture Media, Conditioned
  • DNA Damage
  • Etoposide / toxicity
  • Interleukin-3 / pharmacology*
  • Kinetics
  • Mice
  • Oncogene Protein v-akt
  • Phosphatidylinositol 3-Kinases / metabolism
  • Protein Serine-Threonine Kinases*
  • Protein-Tyrosine Kinases / metabolism
  • Proto-Oncogene Proteins / biosynthesis
  • Proto-Oncogene Proteins / metabolism*
  • Proto-Oncogene Proteins c-akt
  • Recombinant Proteins / biosynthesis
  • Recombinant Proteins / metabolism
  • Retroviridae Proteins, Oncogenic / biosynthesis
  • Retroviridae Proteins, Oncogenic / metabolism*
  • Signal Transduction
  • Thymidine / metabolism
  • Transfection

Substances

  • Culture Media, Conditioned
  • Interleukin-3
  • Proto-Oncogene Proteins
  • Recombinant Proteins
  • Retroviridae Proteins, Oncogenic
  • Etoposide
  • Protein-Tyrosine Kinases
  • Oncogene Protein v-akt
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • Thymidine