GEO series

Synthetic transcription factor overrides persistent repressive chromatin marks [RNA-seq]

GSE196618 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2026/07/02 Platform GPL16791

At a glance

RNA-seq (gene expression) · human · 12 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)
Samples: 12 samples
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)

The prevailing paradigms of epigenetic control posit that signature patterns of post-translational marks on histones guide specific transcriptional outcomes. Methylation of lysine-9 residue of histone H3 (H3K9me3) is implicated in transcriptional silencing through chromatin condensation by its reader HP-1 proteins. Erosion, erasure and subsequent replacement of H3K9me3 by active acetyl-lysine marks accompanies transcriptional up-regulation.

Read the full summary ↓

Here, we report that a synthetic transcription elongation factor (SynTEF1), selectively targets the disease-causing GAA repeat expansion in frataxin and stimulates gene expression without erasure of the signature repressive marks or removal of HP1 proteins. Added epigenetic perturbation with a pharmacological agent leads to supra-synergistic frataxin expression that is unexpectedly accompanied by a dramatic rise in H3K9me3 levels. Active placement of the signature repressive mark is readily overridden by SynTEF1, demonstrating the fluidity and context-dependence of these marks in regulating gene expression. While forcing a reconsideration of how signature epigenetic marks are interpreted, our results provide key insights for therapeutic intervention in rationally reconfiguring disease-associated epigenetic states.

This dataset

Open GSE196618 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 GSE196618_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: 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 PRJNA806168 and SRA study SRP359441. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

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+ 12 more — browse all 12 samples with per-sample file links →

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Search all human RNA-seq datasets in GEO →

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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.