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

GSE286991 Homo sapiens (human) RNA-seq (gene expression) 96 samples Submitted 2026/06/12 Platform GPL18573Platform GPL34284
At a glance

RNA-seq (gene expression) · human · 96 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)
Topic
Acute myeloid leukemiaThis series is part of our curated briefing on it.
Samples
96 samples: 80 distinct titles, 8 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.
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 GSE286991_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 PRJNA1210637 and SRA study SRP557316. Searching any of these in the dataset finder brings you back here.

Study design
80 distinct titles, 8 of them repeated
KDM2B-mAID_5PhIAA ×3 KDM2B-mAID_5PhIAA_GSK343 ×3 KDM2B-mAID_DMSO ×3 KDM2B-mAID_GSK343 ×3 KDM2B-mAID_J2_7_5PhIAA ×3 KDM2B-mAID_J2_7_5PhIAA_GSK343 ×3 KDM2B-mAID_J2_7_DMSO ×3 KDM2B-mAID_J2_7_GSK343 ×3

How we read this: Read from 96 sample titles: 80 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

+ 56 more — browse all 96 samples with per-sample file links →

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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.