Anti-apoptotic activity of the glutathione peroxidase homologue encoded by HIV-1
- UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
- Ethan W Taylor, Senior Research Professor (Creator)
- Institution
- The University of North Carolina at Greensboro (UNCG )
- Web Site: http://library.uncg.edu/
Abstract: The third reading frame of the envelope gene from HIV-1 codes for a protein homologous to the human selenoprotein glutathione peroxidase (GPX). Cells stably or transiently transfected with a HIV-1 GPX construct are protected against the loss of the mitochondrial transmembrane potential and subsequent cell death induced by exogenous reactive oxygen species (ROS) as well as mitochondrion-generated ROS. However, HIV-1 GPX does not confer a general apoptosis resistance, because HIV-1 GPX-transfected cells were not protected against cell death induced by staurosporine or oligomycin. The inhibition of cell death induced by the ROS donor tert-butylhydroperoxide was also observed in cells depleted from endogenous glutathione (GSH), suggesting that GSH is not the sole electron acceptor for HIV-1 GPX. Clinical HIV-1 isolates from long-term non-progressors (untreated patients with diagnosed HIV-1 infection for >10 years, with CD4 T cell count of >500 cells/mm3) mostly possess an intact GPX gene (with only 18% of loss-of-function mutations), while HIV-1 isolates from patients developing AIDS contain non-functional GPX mutants in 9 out of 17 cases (53%). Altogether, these data suggest that HIV-1 GPX possesses a cytoprotective, pathophysiologically relevant function.
Anti-apoptotic activity of the glutathione peroxidase homologue encoded by HIV-1
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Additional Information
- Publication
- Apoptosis 9, 181–192 (2004). https://doi.org/10.1023/B:APPT.0000018800.87358.ba
- Language: English
- Date: 2004
- Keywords
- glutathione, mitochondria, selenium