GEO series
Non-canonical PRC1.1 licenses transcriptional response to enable Treg plasticity in immune adaptation [CUT&TAG]
GSE277417
Homo sapiens; Mus musculus
Genome binding/occupancy profiling by high throughput sequencing
38 samples
Submitted 2026/03/31
Platform GPL24676Platform GPL24247
Summary
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. 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
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Direct links to NCBI, no account and no request form: the whole study as GSE277417_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 38 samples. Raw sequencing reads are also available from ENA.
Also filed as BioProject PRJNA1162137 and SRA study SRP533258. Searching any of these in the dataset finder brings you back here.
Study design
36 conditions, each sampled once — no replicated groups
HEK293T shSCR, H2AK119ub1 CUT&Tag, ×2
HEK293T shKDM2B, H2AK119ub1 CUT&Tag, ×2
Read from 38 sample titles: 36 distinct titles with little repetition. Check it against the sample list below before relying on it.
Samples in this study
0 selected
- GSM7957159 153 KO Treg, H2AK119ub1 CUT&Tag
- GSM7957160 252 KO Treg, H2AK119ub1 CUT&Tag
- GSM7957161 355 WT Treg, H2AK119ub1 CUT&Tag
- GSM7957162 458 WT Treg, H2AK119ub1 CUT&Tag
- GSM7957163 7180 WT Treg, H3K27me3 CUT&Tag
- GSM7957164 7211 WT Treg, H3K27me3 CUT&Tag
- GSM7957165 7199 cKO Treg, H3K27me3 CUT&Tag
- GSM7957166 7181 cKO Treg, H3K27me3 CUT&Tag
- GSM8521992 8441 WT Treg, H3K4me3 CUT&Tag, rep1
- GSM8521993 8443 WT Treg, H3K4me3 CUT&Tag, rep2
- GSM8522002 WT1 Treg, RNAPII-no-1 CUT&Tag, rep1
- GSM8522003 WT2 Treg, RNAPII-no-1 CUT&Tag, rep2
- GSM8522006 HEK293T shSCR, H2AK119ub1 CUT&Tag, rep1
- GSM8522007 HEK293T shSCR, H2AK119ub1 CUT&Tag, rep2
- GSM8522008 HEK293T shKDM2B, H2AK119ub1 CUT&Tag, rep1
- GSM8522009 HEK293T shKDM2B, H2AK119ub1 CUT&Tag, rep2
- GSM8880831 WT Treg-1, KDM2B CUT&Tag, rep1
- GSM8880832 WT Treg-2, KDM2B CUT&Tag, rep2
- GSM8880833 cKO Treg-1, KDM2B CUT&Tag, rep1
- GSM8880834 cKO Treg-2, KDM2B CUT&Tag, rep2
- GSM8880835 WT Treg-1, H3K27ac CUT&Tag, rep1
- GSM8880836 WT Treg-2, H3K27ac CUT&Tag, rep2
- GSM8880839 WT Treg-1, DMSO, 119ub1 CUT&Tag, rep1
- GSM8880840 WT Treg-2, DMSO, 119ub1 CUT&Tag, rep2
- GSM8880841 WT Treg-1, iBP, 119ub1 CUT&Tag, rep1
- GSM8880842 WT Treg-2, iBP, 119ub1 CUT&Tag, rep2
- GSM8880843 WT Treg-1, DMSO, BCOR CUT&Tag, rep1
- GSM8880844 WT Treg-2, DMSO, BCOR CUT&Tag, rep2
- GSM8880845 WT Treg-1, DMSO, KDM2B CUT&Tag, rep1
- GSM8880846 WT Treg-2, DMSO, KDM2B CUT&Tag, rep2
- GSM8880847 WT Treg-1, DMSO, PCGF1 CUT&Tag, rep1
- GSM8880848 WT Treg-2, DMSO, PCGF1 CUT&Tag, rep2
- GSM8880849 WT Treg-1, iBP, BCOR CUT&Tag, rep1
- GSM8880850 WT Treg-2, iBP, BCOR CUT&Tag, rep2
- GSM8880851 WT Treg-1, iBP, KDM2B CUT&Tag, rep1
- GSM8880852 WT Treg-2, iBP, KDM2B CUT&Tag, rep2
- GSM8880853 WT Treg-1, iBP, PCGF1 CUT&Tag, rep1
- GSM8880854 WT Treg-2, iBP, PCGF1 CUT&Tag, rep2
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