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Removal of promoter DNA methylation by epigenome editing reverses HBG silencing [RNA-seq]

GSE284289 Homo sapiens (human) DNA methylation 40 samples Submitted 2025/06/24 Platform GPL24676Platform GPL18573
At a glance

DNA methylation · human · 40 samples

What it is
DNA methylationChemical marks on DNA that help switch genes on or off.
Organism
Homo sapiens (human)
Samples
40 samples: 12 conditions, mostly in triplicateGroups 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
Removal of promoter CpG methylation by epigenome editing reverses HBG silencingNature communications · 2025
Summary (written by the submitters)
Beta-hemoglobinopathies caused by mutations in adult-expressed HBB can be treated by re-activating the adjacent paralogous genes HBG1 and HBG2 (HBG), which are normally silenced perinatally. Although HBG expression is induced by global demethylating drugs, their mechanism is poorly understood and toxicity limits their use. We identified the DNMT1-associated maintenance methylation protein UHRF1 as a mediator of HBG repression in a genome-wide screen.
Read the full summary ↓
Loss of UHRF1 in the adult-type erythroid cell line HUDEP2 caused global demethylation and HBG activation that was reversed upon localized promoter re-methylation. Conversely, targeted demethylation of the HBG promoters activated their genes in HUDEP2 or primary CD34+ cell-derived erythroblasts. Mutation of MBD2, a CpG-methylation reading component of the NuRD complex, to impair methylation sensitivity recapitulated the effects of promoter demethylation. Our studies demonstrate that localized CpG-methylation at the HBG promoters facilitates developmental silencing and identify a targeted therapeutic approach for b-hemoglobinopathies via epigenomic editing.
Published in
Removal of promoter CpG methylation by epigenome editing reverses HBG silencing
Bell HW, Feng R, Shah M et al. · Nature communications 2025 · PMID 40715076 · doi:10.1038/s41467-025-62177-z
This dataset
Open GSE284289 in finder → Find more human 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 GSE284289_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 beta-value tables or raw IDAT files among the supplementary files.

Also filed as BioProject PRJNA1198349 and SRA study SRP551463. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40715076) ↗
Study design
12 conditions, mostly in triplicate
HUDEP-2 WT ×5 HUDEP-2 MBD2Y178F ×5 HUDEP-2 Mock ×3 HUDEP-2 Guide 1 ×3 HUDEP-2 Guide 2 ×3 HUDEP-2 Guide 3 ×3 HUDEP-2 Guide 4 ×3 HUDEP-2 Guide 5 ×3 +4 more

Supports a between-group comparison across 40 samples.

How we read this: 12 replicated groups read from 40 sample titles; they account for 40 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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