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Related Experiment Videos

Cytomegalovirus inhibits p53 nuclear localization signal function.

J Wang1, J D Belcher, P H Marker

  • 1Department of Genetics, Southwest Foundation for Biomedical Research, San Antonio, TX 78227-5301, USA. xwang@darwin.sfbr.org

Journal of Molecular Medicine (Berlin, Germany)
|March 28, 2001
PubMed
Summary

Human cytomegalovirus (CMV) infection prevents p53 from entering the nucleus in endothelial cells, potentially contributing to endothelial dysfunction and atherogenesis. This viral mechanism inactivates p53, impacting cell fate and disease development.

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Area of Science:

  • Virology
  • Cell Biology
  • Cardiovascular Research

Background:

  • Endothelial cells (EC) infected with cytomegalovirus (CMV) exhibit resistance to apoptosis.
  • This resistance may stem from the p53 protein being sequestered in the cytoplasm, preventing its nuclear function.
  • p53 normally functions in the nucleus to regulate apoptosis and cellular responses.

Purpose of the Study:

  • To investigate the hypothesis that CMV infection blocks p53 nuclear localization signal (NLS) function, leading to cytoplasmic sequestration.
  • To understand the role of p53 inactivation in CMV-infected EC dysfunction and atherogenesis.

Main Methods:

  • Transfection of CMV-infected EC with a construct linking p53 NLS inhibitor (NLSI) to chicken muscle pyruvate kinase (PK).
  • Utilizing double-labeling immunofluorescence staining to track the localization of p53 NLSI-conjugated PK.

Related Experiment Videos

  • Assessing the impact of CMV infection stage on NLSI function.

    • Main Results:

    • CMV infection effectively sequesters both PK and p53 in the cytoplasm by inhibiting NLSI function.
    • This inhibition of NLSI is observed during the early and late phases of CMV infection, but not the immediate early phase.
    • The findings indicate a virus-mediated mechanism for p53 inactivation.

    Conclusions:

    • CMV infection inactivates p53 by blocking its nuclear import, contributing to endothelial dysfunction and potentially atherogenesis.
    • This study reveals a novel viral strategy for p53 inactivation, with implications for viral pathogenesis, atherogenesis, and tumorigenesis.