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A CDK11-dependent RNA polymerase II pause-release checkpoint precedes CDK9-mediated transition to transcriptional elongation [RNA-seq]

GSE280102 Homo sapiens (human) RNA-seq (gene expression) 29 samples Submitted 2025/08/25 Platform GPL18573
At a glance

RNA-seq (gene expression) · human · 29 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Samples
29 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
A CDK11-dependent RNA polymerase II pause-checkpoint precedes CDK9-mediated transition to transcriptional elongationMolecular cell · 2025
Summary (written by the submitters)
Controlled gene expression is achieved through the intricate regulation of RNA polymerase II (Pol II) progression through transcription-cycle checkpoints. The pausing checkpoint, where Pol II temporarily stalls prior to release into transcriptional elongation, is a key molecular mechanism that fine-tunes gene expression. While the critical contribution of cyclin-dependent-kinase 9 (CDK9) for Pol II pause-release is well established, the requirement for other CDKs has not been fully elucidated.
Read the full summary ↓
Here we identify a new role for CDK11 in the Pol II pausing-to-elongation transition at a checkpoint that is distinct and independent from CDK9. Selective CDK11 inhibition results in genome-wide stalling of Pol II at transcription-start-site (TSS) proximal regions and acute RNA synthesis ablation near the beginning of transcriptional units. High-resolution chromatin-immunoprecipitation and precision-nuclear-run-on assays reveals spatial differences between CDK11- and CDK9-dependent Pol II pause sites, with CDK11 regulating Pol II closer to the TSS. Cancer cells exhibit profound reliance on functional CDK11, with selective CDK11 inhibition providing therapeutic efficacy in pre-clinical in vivo models of leukaemia and lymphoma, demonstrating the importance of CDK11-dependent Pol II regulation for aggressive haematological malignancies.
Published in
A CDK11-dependent RNA polymerase II pause-checkpoint precedes CDK9-mediated transition to transcriptional elongation
Devlin JR, Martin B, Bartonicek N et al. · Molecular cell 2025 · PMID 40858114 · doi:10.1016/j.molcel.2025.08.001
This dataset
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.

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 GSE280102_RAW.tar (it can run to tens of gigabytes).

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.

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1176462 and SRA study SRP540330. Searching any of these in the dataset finder brings you back here.

Samples in this study

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