GEO series

Targeting CDK12/CYCLIN K induces a gene activation program which is mediated by P-TEFb [ChIP-seq]

GSE316746 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 2 samples Submitted 2026/08/07 Platform GPL30173

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 2 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: 2 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.

Summary (written by the submitters)

Regulation of transcription in human cells is a multistep process controlled by coordinated actions of host transcription factors and their associated kinases. Despite major advances, fundamental gaps still remain in understanding how transcriptional programs are dynamically regulated. Gene expression of Human immunodeficiency virus (HIV) is tightly controlled by the cellular transcription machinery, providing a powerful model for studying transcription regulation.

Read the full summary ↓

Such gene expression regulation is clinically significant, as HIV persists in long-lived reservoirs even under antiretroviral therapy. Here, we show that selective targeting of CDK12/CYCLIN K (CCNK) induces a global gene activation program, which is mediated by positive transcription elongation factor b (P-TEFb). CDK12/CCNK targeting reshapes promoter-proximal and gene bodies landscape at chromatin, and promotes release of P-TEFb from its inhibitory 7SK snRNP complex. Additional transcriptomic profiling reveals preferential upregulation of P-TEFb-target genes, accompanied by induction of relatively short genes and repression of CDK12-regulated DNA damage response pathways. In HIV- infected cells, targeting CDK12/CCNK activates a robust viral gene expression, accompanied with latency reversal and importantly, synergistic reactivation effects when combined with latency- reversing agents. Together, these results uncover a previously unrecognized compensatory interplay between transcriptional kinases that rewires the cellular gene expression program with implications for HIV latency reversal and cancer biology.

This dataset

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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 GSE316746_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 PRJNA1404119 and SRA study SRP663474. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

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+ 2 more — browse all 2 samples with per-sample file links →

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