Journal
JOURNAL OF VIROLOGY
Volume 83, Issue 19, Pages 10256-10263Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.02654-08
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Funding
- INSERM
- CNRS
- Universite Paris-Descartes
- French National Agency for AIDS Research (ANRS)
- National Programme for Research in Functional Genomics in Norway
- Research Council of Norway
- Norwegian Cancer Society
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It was recently reported that human immunodeficiency virus type 1 (HIV-1) Vpr induced the proteasomal degradation of the nuclear UNG2 enzyme for efficient virus replication. We confirm here that HIV-1 infection and Vpr expression reduce the level of endogenous UNG2, but this effect is not reverted by treatment with the proteasome inhibitor MG132. Moreover, this reduction is not mediated by Vpr binding to UNG2 and is independent of the Vpr-induced G2 arrest. Finally, we show that Vpr influences the UNG2 promoter without affecting UNG1 gene expression. These data indicate that the Vpr-induced decrease of UNG2 level is mainly related to a transcriptional effect.
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