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p48 Overexpression enhances interferon-mediated expression and activity of double-stranded RNA-dependent protein

Yoko Tamada1, Kazuhiko Nakao, Yuji Nagayama

  • 1Department of Clinical Pharmacology, Nagasaki University, 1-7-1 Sakamoto, Nagasaki 852-8501, Japan.

Journal of Hepatology
|September 10, 2002
PubMed
Abstract

Insights

p48 gene transduction enhances interferon-alpha-induced double-stranded RNA-dependent protein kinase (PKR) expression and activity in liver cells. This combination blocks protein synthesis without affecting mRNA levels, suggesting a potential antiviral strategy.

Area of Science:

  • Hepatology
  • Virology
  • Molecular Biology

Background:

  • Double-stranded RNA-dependent protein kinase (PKR) mediates interferon (IFN)-induced antiviral responses.
  • p48, alongside STAT1 and STAT2, is crucial for IFN-alpha signaling.

Purpose of the Study:

  • To investigate the impact of p48 gene transduction on PKR expression and activity in HuH-7 human hepatoma cells.

Main Methods:

  • HuH-7 cells were transduced with p48 gene via adenoviral or plasmid vectors.
  • Cells were treated with or without IFN-alpha.
  • PKR expression, eIF2alpha phosphorylation, and protein translation inhibition (CAT gene, alpha-fetoprotein) were assessed.

Main Results:

  • p48 overexpression alone did not increase PKR expression.
  • Combined p48 overexpression and IFN-alpha treatment significantly elevated PKR expression and eIF2alpha phosphorylation.
  • This led to blocked translation of transfected CAT and endogenous alpha-fetoprotein without altering mRNA levels.

Conclusions:

  • p48 gene transduction can enhance IFN-mediated PKR expression and activity in hepatocytes.
  • This approach may offer a strategy for boosting antiviral responses in liver cells.

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