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Sustained PRC1.1 activity preserves gene repression independently of PRC2.2 and restrains leukemic cell differentiation

GSE286993 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 21 samples Submitted 2026/06/12 Platform GPL18573
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 21 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
21 samples: 8 conditions, mostly in duplicateGroups 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
Sustained PRC1.1 activity preserves gene repression independently of PRC2.2 and restrains leukemic cell differentiationNucleic acids research · 2026
Summary (written by the submitters)
Loss-of-function mutations in BCOR, a subunit of the non-canonical Polycomb Repressive Complex 1.1 (PRC1.1), are frequently observed in acute myeloid leukemia (AML) and associate with adverse risk. Paradoxically, leukemic stem cell viability in BCOR wild type AMLs strongly depends on PRC1.1 activity. Here, we use BCOR and KDM2B degron models to study PRC1.1 dependency in leukemic cells and find that BCOR is a bridging factor tethering the catalytic and chromatin-binding moieties of the PRC1.1 complex.
Read the full summary ↓
BCOR degradation induces a quick localized loss of H2AK119ub at PRC1.1 target genes, whereas PRC2-induced H3K27me3 remains unaffected. Degron-mediated depletion of BCOR or KDM2B induces a rapid but time-dependent transcriptional induction, whereby late-upregulated genes are more heavily decorated with H3K27me3 compared to early-upregulated genes. Combined PRC1.1 inactivation and PRC2 inhibition further amplifies gene induction suggesting collaborative yet distinct control over target genes. Strikingly, both JARID2/AEBP2 and SUZ12 knockout cells, devoid of PRC2.2 or PRC2.1/PRC2.2 respectively, retain PRC1.1 loss-induced transcriptional activation, underscoring that PRC1.1 can repress target genes independently of a downstream PRC2.2-canonical PRC1 repressive axis. Finally, combined targeting of PRC1.1 and PRC2 induces differentiation of leukemic cells emphasizing that co-targeting PRC1.1 and PRC2 represents a promising strategy to improve treatment of AML patients.
Published in
Sustained PRC1.1 activity preserves gene repression independently of PRC2.2 and restrains leukemic cell differentiation
Mojallali F, De Meis A, Alkema SG et al. · Nucleic acids research 2026 · PMID 42273916 · doi:10.1093/nar/gkag529
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 GSE286993_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1210639 and SRA study SRP557319. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, mostly in duplicate
K562_BCOR_8hDMSO_H2AK119ub ×2 K562_BCOR_8h5phIAA_H2AK119ub ×2 K562_BCOR_8hDMSO_H3K27me3 ×2 K562_BCOR_8h5phIAA_H3K27me3 ×2 K562_BCOR_8hDMSO_H3K27ac ×2 K562_BCOR_8h5phIAA_H3K27ac ×2 K562_BCOR_8hDMSO_H3K4me3 ×2 K562_BCOR_8h5phIAA_H3K4me3 ×2 +5 more

Supports a between-group comparison across 16 samples.

How we read this: 8 replicated groups read from 21 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
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