The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.
The human immunodeficiency virus type 1 vpr gene arrests infected T cells in the G2 + M phase of the cell cycle
Open accessAbstract
Human immunodeficiency virus type 1 (HIV-1) infection causes profound immunological defects in afflicted patients. Various mechanisms have been proposed to account for the immune dysfunction in AIDS ultimately leading to loss of CD4+ T cells, including HIV-1 envelope-mediated syncytium formation, apoptosis, and cytokine modulation. Here we present results which suggest a novel hypothesis for T-cell dysfunction. We show, using HIV-1 bearing a novel cell surface reporter gene, that infected cells are unable to progress normally through the cell cycle and became arrested in the G2 + M phase. Furthermore, we identify the HIV-1 vpr gene product as being both necessary and sufficient for eliciting this cell cycle arrest. Cell cycle arrest induced by Vpr correlates with an increase in the hyperphosphorylated (inactive) form of the cyclin-dependent serine/threonine kinase CDC2, consistent with an arrest of cells at the boundary of G2 and M.
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Cites
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Structural biology of HIV 1 1Edited by P. E. Wright
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Stable gene transfer to the nervous system using a non-primate lentiviral vector
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HIV-1 Vpr-Mediated G2 Arrest Involves the DDB1-CUL4AVPRBP E3 Ubiquitin Ligase
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Self-citation
Metadata
- Authors
- Jowett, J. B., Planelles, V, Poon, B., Shah, N. P., Chen, M. L., & Chen, I. S.
- Venue
- Journal of Virology
- Publisher
- American Society for Microbiology
- Published
- 1995-10
- Volume
- 69
- Issue
- 10
- Pages
- 6304-6313
- ISSN
- 0022-538X (ISSN-L)
- 1098-5514
- OpenAlex
- W1480448067
- Cited by
- 526
- References
- 59
- FWCI
- 8.28
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Jowett, J. B., Planelles, V, Poon, B., Shah, N. P., Chen, M. L., & Chen, I. S. (1995). The human immunodeficiency virus type 1 vpr gene arrests infected T cells in the G2 + M phase of the cell cycle. Journal of Virology. https://doi.org/10.1128/jvi.69.10.6304-6313.1995
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