Abstract
The p14ARF tumor suppressor functions as 'oncogenic checkpoint' that prevents unrestricted cellular proliferation in response to oncogenic signaling. Albeit, the major pathway through which ARF operates is the ARF-Mdm2-p53 axis, ARF directly binds to and inactivates transcription function of a number of DNA-bound activators. In the present study we show that p14 ARF inhibits transcription activation of HIV-1 LTR promoter activity by Tat protein. Tat protein is a RNA-bound transcriptional activator whose function is strictly required for HIV-1 replication. We determined that p14 ARF inhibits Tat transactivation of HIV-1 LTR by promoting Tat degradation via an ubiquitin-independent pathway.
Original language | English |
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Pages (from-to) | 1433-1439 |
Number of pages | 7 |
Journal | Cell Cycle |
Volume | 7 |
Issue number | 10 |
Publication status | Published - May 15 2008 |
Keywords
- Degradation
- Gene expression
- Inhibition
- Oncosuppressor
- p14
- Tat
- Ubiquitination
ASJC Scopus subject areas
- Cell Biology
- Biochemistry
- Molecular Biology
- Medicine(all)