Regulation of the Interferon-Induced PKR: Can Viruses Cope?

Trends Microbiol. 1995 Feb;3(2):75-8. doi: 10.1016/s0966-842x(00)88880-0.

Abstract

Viruses that fail to block the lethal effects of the double-stranded-RNA-activated protein kinase (PKR) may be doomed; why do so many viruses go to so much trouble to downregulate this interferon-induced protein kinase? PKR may regulate cell growth and proliferation in uninfected cells, suggesting that it also participates in the antiproliferative arm of the interferon response.

Publication types

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

MeSH terms

  • Animals
  • Cell Transformation, Neoplastic
  • Enzyme Induction
  • Gene Expression Regulation, Viral*
  • HSP40 Heat-Shock Proteins
  • Humans
  • Interferons / physiology*
  • Protein-Serine-Threonine Kinases / antagonists & inhibitors
  • Protein-Serine-Threonine Kinases / physiology*
  • Repressor Proteins / physiology
  • Virus Physiological Phenomena*
  • eIF-2 Kinase

Substances

  • DNAJC3 protein, human
  • HSP40 Heat-Shock Proteins
  • Repressor Proteins
  • Interferons
  • Protein-Serine-Threonine Kinases
  • eIF-2 Kinase