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Decoding Gene Responsiveness to Synthetic Chromatin Reader-Actuators with Multi-Modal Epigenomic Profiling

GSE333192 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 38 samples Submitted 2026/05/29 Platform GPL24676
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: 16 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.
Summary (written by the submitters)
Cell identity is regulated by chromatin states that encode gene regulatory memory and shape responses to new inputs. To investigate how chromatin context influences inducibility in differentiated cells, we employed engineered synthetic reader-actuators (SRAs), fusion proteins containing the polycomb chromodomain (PCD) that binds H3K27me3.
Read the full summary ↓
In MCF7 breast cancer cells, we mapped PCD-fusion occupancy by ChIP-seq and used RNA-seq to identify temporally resolved gene activation patterns. ChIP-seq profiling and machine learning models (MLM) demonstrated that PCD-fusion binding was predicted primarily by the absence of H3K4me3 or H3K9ac enrichment, suggesting selective accessibility at enhancers and chromatin transition zones. Among genes with SRA-enriched enhancers, the SRA-induced subset was distinguished by promoter features including bivalent histone modifications and enrichment of transcription factors NEUROD1 and MTA1. Collectively, our results demonstrate that SRA responsiveness depends on a specific chromatin signature beyond H3K27me3 alone. This study demonstrates the power of SRAs to dissect inducible chromatin features in their native genomic context, and suggests that epigenetically repressed regions in differentiated cells can retain regulatory plasticity.
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 GSE333192_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 PRJNA1469638. Searching any of these in the dataset finder brings you back here.

Study design
16 conditions, mostly in duplicate
MCF7 uninduced RFP-VP64 transgene ×3 MCF7 uninduced PCD-RFP transgene ×3 MCF7 24h dox-induced PCD-RFP transgene ×3 MCF7 uninduced SRA transgene ×3 MCF7 24h dox-induced SRA transgene ×3 MCF7 48h dox-induced SRA transgene ×3 MCF7 dox-induced CBX8PCD-RFP transgene anti-m… ×2 MCF7 dox-induced CBX8PCD-RFP transgene ChIP i… ×2 +8 more

Supports a between-group comparison across 38 samples.

How we read this: 16 replicated groups read from 38 sample titles; they account for 38 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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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.