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Unleashed condensation by recurrent mutations of an epigenetic regulator promotes cancer

GSE264442 Mus musculus (mouse) RNA-seq (gene expression) 16 samples Submitted 2026/04/23 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 16 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
Mus musculus (mouse)
Samples
16 samples: 10 × Ck0315 vs 6 × Ck0201Groups 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.
Paper
Unleashed condensation by recurrent mutations of an epigenetic regulator promotes cancerbioRxiv : the preprint server for biology · 2026
Summary (written by the submitters)
The pathological mechanisms and significance for the prevalent mutation hotspots in disordered protein regions are poorly understood. ASXL1 is an obligate co-factor for BAP1 in H2AK119 deubiquitination. ASXL1 mutations are very frequent in myeloid malignancies, and are mostly C-terminal truncating mutations concentrated in a specific disordered region of ASXL1.
Read the full summary ↓
ASXL1 truncations are gain-of-function mutations that promote myeloid malignancies, but the underlying mechanisms remain poorly understood. Here we show that the frequently truncated mutants of ASXL1 possess an intrinsic property of forming phase-separated biomolecular condensates, and this property is normally suppressed by the frequently deleted regions. A disease-mutant of the endogenous ASXL1 in leukemia cells forms dynamic nuclear co-condensates with other endogenous factors important for gene activation. While the ASXL1 disease-mutant can greatly enhance H2A deubiquitination activity of BAP1 in cells and in a purified system, enhance the growth of myeloid leukemia cell growth, and promote hematopoietic colony formation and leukemogenesis in a mouse transplant model by turning on myeloid leukemogenic transcriptional programs, substitution of residues important for condensation disrupted or impaired these abilities, suggesting that the condensation property is crucially important for the ASXL1 mutants in promoting cancer. Moreover, we discover that the conserved negative charges in the highly disordered and frequently deleted region on ASXL1 suppress the condensation of the wild type ASXL1. Charge-neutralizing mutations in this region restores condensation of the full-length ASXL1, and renders the full-length protein capable of promoting leukemogenesis-associated activity and gene expression. Biochemical, biophysical, and simulation analyses suggest the intramolecular interactions normally mask the N-terminal region in engaging intermolecular interactions required for phase separation, and disease truncations escape from the regulatory interactions and unleash the phase separation property to form nuclear hubs to promote expression of tumorigenic gene programs. Finally, by showing a striking correlation of the mutation frequencies with the condensation properties and leukemogenesis activity for a series of human patient mutations, we suggest that dysregulation of condensation is a likely a central mechanism for ASXL1 mutations in promoting myeloid malignancies. This may also be an overlooked mechanism for the prevalent hotspot disease mutations in the disordered proteomes.
Published in
Unleashed condensation by recurrent mutations of an epigenetic regulator promotes cancer
Song Y, Hao Y, Latacz M et al. · bioRxiv : the preprint server for biology 2026 · PMID 41756950 · doi:10.64898/2026.02.18.706652
This dataset
Open GSE264442 in finder → Find more mouse RNA-seq 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 GSE264442_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: 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 PRJNA1102416 and SRA study SRP502913. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41756950) ↗
Study design
10 × Ck0315 vs 6 × Ck0201

Supports a between-group comparison across 16 samples.

How we read this: 2 replicated groups read from 16 sample titles; they account for 16 of them. 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
Datasets on a similar topic

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