The interferon-induced double-stranded RNA-activated protein kinase induces apoptosis

Virology. 1994 Mar;199(2):491-6. doi: 10.1006/viro.1994.1151.


Interferons (IFNs) exert antitumor activities, but the molecular mechanism underlying these effects is poorly understood. IFN-induced, double-stranded (ds) RNA-activated protein kinase (p68 kinase) has long been implicated in mediating the antiproliferative effects of IFN. In addition, recent studies suggest that p68 kinase may function as a tumor suppressor gene. In this investigation we showed that expression of p68 kinase in HeLa cells resulted in a rapid cell death characteristic of apoptosis. Rapid cell death was not observed in cells which expressed a mutant form of p68 kinase (lys296-->arg) indicating that cell death observed is the result of p68 kinase expression and activation. Moreover, infection of HeLa cells with the mutant vaccinia virus lacking E3L gene, which encodes a dsRNA binding protein that acts as an inhibitor of p68 kinase, also resulted in apoptosis. Thus, we propose that human p68 kinase functions as a tumor suppressor gene by actively participating in apoptosis.

Publication types

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

MeSH terms

  • Apoptosis / physiology*
  • HeLa Cells
  • Humans
  • Interferons / pharmacology
  • Mutation
  • Protein-Serine-Threonine Kinases / biosynthesis
  • Protein-Serine-Threonine Kinases / genetics
  • Protein-Serine-Threonine Kinases / physiology*
  • Recombinant Proteins / biosynthesis
  • Vaccinia virus
  • eIF-2 Kinase


  • Recombinant Proteins
  • Interferons
  • Protein-Serine-Threonine Kinases
  • eIF-2 Kinase