ArticleNucleic acids research2025
The p400 complex promotes HIV-1 latency by suppressing viral transcription and altering the host cell state.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Quantitative limits of host-driven HIV transcription and host gene control by the viral transactivator Tat.Nucleic acids research · 2026Article
- The human chromatin remodeling complex p400 restricts HIV-1 transcription in a Tat-dependent manner.Nucleic acids research · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Eradicating HIV-1 is complicated by latently infected CD4+T cells harboring dormant proviruses capable of reactivation. Through a pooled shRNAmir screen targeting human chromatin regulators, we identified EP400, a member of the p400 chromatin remodeling complex, as a potent inhibitor of HIV-1 transcription in Jurkat and primary CD4+T cells. EP400 and its complex partner DMAP1 co-localize with paused RNA Polymerase II (RNAPII) at transcriptional start sites of protein-coding genes and their depletion modestly reduced RNAPII pausing. At the HIV-1 locus, EP400 and DMAP1 were co-recruited with RNAPII across the entire HIV-1 genome, and their depletion markedly increases RNAPII pause release. Together this suggests that EP400 may play a role in limiting HIV-1 transcriptional elongation. Additionally, EP400 depletion increased expression of key T-cell factors known to activate HIV-1 transcription. Therefore, the p400 complex reduces efficient HIV-1 transcriptional elongation and contributes to a CD4+T cell state unfavorable for HIV-1 transcription.
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