HIV transcriptional activation by the accessory protein, VPR, is mediated by the p300 co-activator.

The accessory protein, Vpr, is a virion-associated protein that is required for HIV-1 replication in macrophages and regulates viral gene expression in T cells. Vpr causes arrest of cell cycle progression at G2/M, presumably through its effect on cyclin B1.Cdc2 activity. Here, we show that the ability of Vpr to ...
activate HIV transcription correlates with its ability to induce G2/M growth arrest, and this effect is mediated by the p300 transcriptional co-activator, which promotes cooperative interactions between the Rel A subunit of NF-kappaB and cyclin B1.Cdc2. Vpr cooperates with p300, which regulates NF-kappaB and the basal transcriptional machinery, to increase HIV gene expression. Similar effects are seen in the absence of Vpr with a kinase-deficient Cdc2, and overexpression of p300 increases levels of HIV Vpr+ replication. Taken together, these data suggest that p300, through its interactions with NF-kappaB, basal transcriptional components, and Cdks, is modulated by Vpr and regulates HIV replication. The regulation of p300 by Vpr provides a mechanism to enhance viral replication in proliferating cells after growth arrest by increasing viral transcription.
Mesh Terms:
CDC2 Protein Kinase, CREB-Binding Protein, Cell Cycle, Gene Expression Regulation, Viral, Gene Products, vpr, HIV-1, Humans, Jurkat Cells, Nuclear Proteins, Trans-Activators, Transcription Factors, Transcription, Genetic, Virus Replication, vpr Gene Products, Human Immunodeficiency Virus
Proc. Natl. Acad. Sci. U.S.A.
Date: Apr. 28, 1998
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