The role of Tat in the human immunodeficiency virus life cycle indicates a primary effect on transcriptional elongation.
- 1 May 1991
- journal article
- research article
- Published by Proceedings of the National Academy of Sciences in Proceedings of the National Academy of Sciences
- Vol. 88 (9) , 4045-4049
- https://doi.org/10.1073/pnas.88.9.4045
Abstract
The mechanism of Tat transactivation was studied by treating cell lines containing Tat-defective viruses with purified Tat protein. These cell lines constitutively produce very low levels of virus in the absence of Tat, as measured by p24 antigen levels. Virus production can be increased greater than 30,000-fold by adding exogenous Tat. Tat addition increases mRNA levels early in the viral life cycle, and Tat is required for Rev function to become evident. There is no evidence for a translational effect of Tat. Nuclear run-on experiments show that the increase in mRNA levels is due to an increased efficiency of elongation of nascent transcripts. These results suggest that Tat may be a gene-specific elongation factor.Keywords
This publication has 36 references indexed in Scilit:
- Synergy between HIV-1 Tat and adenovirus E1A is principally due to stabilization of transcriptional elongation.Genes & Development, 1990
- Messenger RNA Transport and HIV rev RegulationScience, 1990
- Inhibition of Antigen-Induced Lymphocyte Proliferation by Tat Protein from HIV-1Science, 1989
- In vitro formation of short RNA polymerase II transcripts that terminate within the HIV-1 and HIV-2 promoter-proximal downstream regions.Genes & Development, 1989
- Cellular uptake of the tat protein from human immunodeficiency virusCell, 1988
- Transcriptional but not translational regulation of HIV-1 by the tat gene productNature, 1988
- Expression and Characterization of the Trans -Activator of HTLV-III/LAV VirusScience, 1986
- Trans-activation of human immunodeficiency virus occurs via a bimodal mechanismCell, 1986
- The location of cis-acting regulatory sequences in the human T cell lymphotropic virus type III (HTLV-III/LAV) long terminal repeatCell, 1985
- Stimulation of 3T3 cells induces transcription of the c-fos proto-oncogeneNature, 1984