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Updated: Oct 23, 2026

Studying RNA Interactors of Protein Kinase RNA-Activated during the Mammalian Cell Cycle
10:05

Studying RNA Interactors of Protein Kinase RNA-Activated during the Mammalian Cell Cycle

Published on: March 5, 2019

Regulatable expression of the interferon-induced double-stranded RNA dependent protein kinase PKR induces apoptosis

O Donzé1, J Dostie, N Sonenberg

  • 1Department of Biochemistry and McGill Cancer Center, McGill University, 3655 Drummond Street, Montréal, Québec, H3G1Y6, Canada. Donzé/2/sc2a,unige.ch

Virology
|April 7, 1999
PubMed

Insights

The protein kinase R (PKR) triggers apoptosis, or programmed cell death, when expressed in cells. This process may involve the upregulation of the Fas receptor, a key component in cell death signaling pathways.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Immunology

Background:

  • Protein kinase R (PKR) is an interferon-induced enzyme.
  • PKR plays a role in antiviral responses, cell growth, differentiation, tumor suppression, and apoptosis.
  • Previous functional studies of PKR were limited by the absence of a suitable expression system.

Purpose of the Study:

  • To investigate the role of PKR in programmed cell death (apoptosis).
  • To establish a functional expression system for PKR in NIH3T3 cells using a tetracycline-regulated system.

Main Methods:

  • Utilized a tetracycline-regulated inducible expression system in NIH3T3 cells.
  • Expressed wild-type PKR and an inactive mutant (K296R).
  • Monitored apoptosis induction and Fas receptor mRNA levels.

Main Results:

  • Expression of wild-type PKR induced apoptosis in NIH3T3 cells.
  • PKR expression correlated with increased Fas receptor mRNA levels.
  • Inactive PKR mutant or vector alone did not induce apoptosis or affect Fas mRNA levels.

Conclusions:

  • Active PKR expression triggers apoptosis.
  • Apoptosis induction by PKR may occur through the upregulation of the Fas receptor.
  • A tetracycline-regulated system is effective for studying PKR function in apoptosis.

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