ArticleVirus genes2010
Over-expression of the HIV-1 Rev promotes death of nondividing eukaryotic cells.
Article in Virus genes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Molecular characterization of HIV-1 genome in fission yeast Schizosaccharomyces pombe.Cell & bioscience · 2015Article
- Article
- Specific eradication of HIV-1 from infected cultured cells.AIDS research and therapy · 2010Article
- Peptides derived from the HIV-1 integrase promote HIV-1 infection and multi-integration of viral cDNA in LEDGF/p75-knockdown cells.Virology journal · 2010Article
- A novel role for the viral Rev protein in promoting resistance to superinfection by human immunodeficiency virus type 1.The Journal of general virology · 2010Article
- Transportin 3 and importin α are required for effective nuclear import of HIV-1 integrase in virus-infected cells.Nucleus (Austin, Tex.)Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of the human immunodeficiency virus type 1 (HIV-1) Rev protein is essential for completion of the viral life cycle. Rev mediates nuclear export of partially spliced and unspliced viral transcripts and therefore bears a nuclear localization signal (NLS) as well as a nuclear export signal (NES), which allow its nucleocytoplasmic shuttling. Attempts to express the wild-type Rev protein in eukaryotic human cultured cells have encountered difficulties and so far have failed. Here we show that accumulation of Rev, which occurs in nondividing Rev-expressing cells or when such cells reach confluency, results in death of these cells. Cell death was also promoted by addition of a cell permeable peptide bearing the Rev-NES sequence, but not by the Rev-NLS peptide. Our results probably indicate that binding of excess amounts of the Rev protein or the NES peptide to the exportin receptor CRM1 results in cells' death.
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Registered trials
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