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

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The dsRNA protein kinase PKR: virus and cell control

M A García1, E F Meurs, M Esteban

  • 1Department of Molecular and Cellular Biology, Centro Nacional de Biotecnología, CSIC, Ciudad Universitaria Cantoblanco, 28049 Madrid, Spain.

Biochimie
|April 25, 2007
PubMed

Insights

Double-stranded RNA-dependent protein kinase (PKR) inhibits viral replication by halting protein translation. Viruses have evolved inhibitors, while cellular proteins modulate PKR

Area of Science:

  • Molecular Biology
  • Virology
  • Cellular Stress Response

Background:

  • Double-stranded RNA-dependent protein kinase (PKR) is a mammalian serine-threonine kinase.
  • PKR phosphorylates the eIF2 alpha translation initiation factor in response to stress, primarily viral infections.
  • eIF2 alpha phosphorylation arrests translation, inhibiting viral replication.

Purpose of the Study:

  • To elucidate the activation mechanism and regulatory network of PKR.
  • To understand PKR's role in antiviral defense and apoptosis.
  • To explore PKR's influence on cell growth and differentiation.

Main Methods:

  • Analysis of PKR activation via dsRNA binding motifs (dsRBM).
  • Investigation of viral PKR inhibitors (e.g., Vaccinia E3L, K3L).
  • Examination of cellular protein regulation (positive and negative modulators).
  • Study of PKR's role in apoptosis pathways (FADD/caspase 8, APAF/caspase 9).
  • Assessment of PKR's impact on translation, transcription, cell growth, and differentiation.

Main Results:

  • PKR activation is triggered by dsRNA binding through its N-terminal dsRBM.
  • Viruses employ inhibitors like Vaccinia E3L/K3L to counteract PKR.
  • Cellular proteins (e.g., RAX/PACT, Mda7, p58IPK) modulate PKR activity.
  • PKR induces apoptosis via caspase pathways and influences NF-kappaB, ATF-3, and p53.
  • PKR impacts cell growth, differentiation, and is linked to oncogenes.

Conclusions:

  • PKR is a critical component of the innate antiviral response.
  • Its activity is tightly regulated by viral and cellular factors.
  • PKR plays a multifaceted role in cellular processes including apoptosis and growth control.

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