GEO series

The p400 complex promotes HIV-1 latency by suppressing 1 viral transcription and altering the host cell state [ChIP-seq]

GSE280359 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 80 samples Submitted 2025/08/19 Platform GPL18573Platform GPL30173

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 80 samples

What it is: ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism: Homo sapiens (human)
Samples: 80 samples
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper: The p400 complex promotes HIV-1 latency by suppressing viral transcription and altering the host cell stateNucleic acids research · 2025

Summary (written by the submitters)

Eradicating HIV-1 is complicated by latently infected CD4+T cells harboring repressed HIV-1 proviruses that can reactivate. Using a pooled shRNAmir screen of all human chromatin regulators we identified previously unappreciated factors that govern HIV-1 latency and reactivation. Depletion of EP400 and DMAP1, core subunits of the multifunctional p400 complex, strongly derepressed HIV-1 transcription in Jurkat and primary CD4+T cells.

Read the full summary ↓

EP400/DMAP1 co-localize with paused RNA Polymerase II (RNAPII) at the transcriptional start sites (TSS) of protein-coding genes, limiting RNAPII pause release, with HIV-1 elongation particularly affected. TNF-⍺ stimulation robustly promotes co-recruitment of RNAPII, EP400, and DMAP1 across the HIV-1 genome, which is distinct from other genes where this co-recruitment occurs mainly at the TSS. Depletion of EP400/DMAP1 reactivated HIV transcription independently of histone variant exchange and KAT5 activity, and increased gene expression of key T cell factors known to trans-activate HIV-1. Thus, the p400 complex is a host restriction factor that blocks RNAPII transcriptional elongation at the HIV-1 locus and creates a CD4+T cell state unfavorable for HIV-1 transcription.

Published in

The p400 complex promotes HIV-1 latency by suppressing viral transcription and altering the host cell state

Mori LP, Li C, Venables T et al. · Nucleic acids research 2025 · PMID 40842241 · doi:10.1093/nar/gkaf764

This dataset

Open GSE280359 in finder → Find more human ChIP / ATAC / CUT&Tag datasets →

Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE280359_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1177981 and SRA study SRP540947. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40842241) ↗

Samples in this study

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+ 80 more — browse all 80 samples with per-sample file links →

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