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Non-canonical PRC1.1 licenses transcriptional response to enable Treg plasticity in immune adaptation [CUT&TAG]

GSE277417 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 38 samples Submitted 2026/03/31 Platform GPL24676Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 38 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
38 samples: 36 distinct titles, 2 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)
Polycomb Repressive Complexes (PRCs) sustain regulatory T (Treg) cell identity through transcriptional silencing, yet their role in modulating Treg functional plasticity during immune adaptation remains unclear. Here, we identify KDM2B, a defining component of non-canonical PRC1.1, as a critical regulator for sustaining the proportion and immunosuppressive functions of active Treg (aTreg) cells without altering Treg abundance or identity.
Read the full summary ↓
Mechanistically, PRC1.1 deposits H2AK119 monoubiquitylation (H2AK119ub1) at active promoters, surprisingly licensing aTreg transcriptional programs beyond its repressive role. Disruption of PRC1.1 via Kdm2b ablation or pharmacological inhibition with iBP, a novel selective inhibitor, reduces H2AK119ub1, blunts stimulus-dependent transcriptional activation and suppresses Treg activation. Notably, Treg-specific Kdm2b deletion in melanoma-bearing mice enhances anti-tumor immunity and synergizes with anti-PD-L1 therapy. Therefore, our study redefines H2AK119ub1 as a dual-function epigenetic mark and PRC1.1 as a molecular rheostat fine-tuning Treg adaptability, establishing PRC1.1 as a therapeutic target to decouple immune suppression in cancer while preserving Treg homeostasis.
This dataset
Open GSE277417 in finder → Find more 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 GSE277417_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 PRJNA1162137 and SRA study SRP533258. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
36 distinct titles, 2 of them repeated
HEK293T shSCR, H2AK119ub1 CUT&Tag, ×2 HEK293T shKDM2B, H2AK119ub1 CUT&Tag, ×2

How we read this: Read from 38 sample titles: 36 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
Datasets on a similar topic

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