GEO series

Transcriptional condensates enrich phosphorylated PRMT2 to stimulate H3R8me2a deposition and hypoxic response in cancers- Cut&tag

GSE262583 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 10 samples Submitted 2026/01/01 Platform GPL24676

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 10 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: 10 samples: 9 distinct titles, 1 of them repeatedGroups are read from the sample names, not from the paper. Check the list below.
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)

Histone arginine methylation, catalyzed by protein arginine methyltransferases (PRMTs), is crucial for transcription regulation and increasingly associated with cancer progression. However, some PRMTs present challenges as drug targets due to their unique, context-dependent activities. Here we report that hypoxia induces rapid condensation of PRMT2, which is required for its activity on histone H3R8 asymmetric dimethylation (H3R8me2a).

Read the full summary ↓

Consistent with its roles in transcription activation, PRMT2 is enriched in transcriptional condensates and relies on its phosphorylation at Ser 12 (PRMT2S12ph). This phosphorylation, situated within the N-terminal intrinsic disordered regions of PRMT2, facilitates its integration into transcriptional condensates and H3R8me2a deposition. Consequently, PRMT2S12 phosphorylation is indispensable for transcription activation of the hypoxia-inducible genes and tumor progression in vivo. Notably, transcription-associated Cyclin-Dependent Kinases (CDK7-CDK9) is imperative for PRMT2S12 phosphorylation. As a result, CDK9 inhibitors suppress hypoxia-induced H3R8me2a activity and transcription, and they synergize with Temozolomide (TMZ) in halting tumor progression, partly reliant on blocking PRMT2S12ph. Therefore, our study uncovers novel roles of transcriptional condensation in augmenting methyltransferase activity and provide a fresh anti-cancer mechanism for CDK9 inhibitors by restricting context-dependent transcriptional programs.

This dataset

Open GSE262583 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 GSE262583_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 PRJNA1092594 and SRA study SRP498128. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

9 distinct titles, 1 of them repeated

control-Hyp ×2

How we read this: Read from 10 sample titles: 9 distinct titles with little repetition. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

GSM8172022 control-Hyp
GSM8172023 control-Nor
GSM8172024 control-TG02
GSM8172025 PRMT2-S12A Hyp
GSM8172026 PRMT2-WT Hyp
GSM8726101 control-Hyp-2
GSM8726102 control-Nor-2
GSM8726103 control-TG02-Hyp-2
GSM8726104 H3R8me2a-PRMT2-S12A-Hyp-2
GSM8726105 H3R8me2a-PRMT2-WT-Hyp-2

Datasets on a similar topic

GSE262581 Transcriptional condensates enrich phosphorylated PRMT2 to stimulate H3R8me2a deposition and hypoxic response in cancers-RNA-seq 8 samples shares h3r8me2a, prmt2, phosphorylated, condensates, deposition, stimulate, hypoxic, enrich
GSE334988 Transcriptomic profiling of PRMT2 wild-type and PRMT2 knockout KG-1a acute myeloid leukemia cells 9 samples shares prmt2
GSE266252 Effect of depletion of PRMT2 on gene expression in the HL-60 acute myeloid leukemia cell line 9 samples shares prmt2
GSE235438 Hypoxia-inducible PRMT2 addiction in cancers 3 samples shares prmt2
GSE273678 Phase-separated NDF−FACT condensates facilitate transcription elongation on chromatin [ChIP-Seq] 55 samples shares condensates
GSE302795 Phosphorylated ubiquitin is a secondary messenger and an epigenetic mark mediating mitochondria-nucleus crosstalk 54 samples shares phosphorylated
GSE243824 Mechanism for controlled assembly of transcriptional condensates by Aire [ChIP-seq] 46 samples shares condensates
GSE281165 TFE3 fusion oncoprotein condensates drive epigenetic reprogramming and cancer progression [CUT&RUN] 43 samples shares condensates

Search all human ChIP / ATAC / CUT&Tag datasets in GEO →

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.