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DUX4 activates a transcriptional network involving Krüppel-like factors KLF17 and KLF18 [KLF17_KLF18_OE]

GSE299603 Homo sapiens (human) RNA-seq (gene expression) 9 samples Submitted 2026/06/10 Platform GPL34284
At a glance

RNA-seq (gene expression) · human · 9 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
9 samples: 3 × MB135 KLF17 vs 3 × MB135 KLF18 vs 3 × MB135 GFPGroups 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)
DUX4 is a critical regulator of gene expression during human embryonic development and is the driver of facioscapulohumeral muscular dystrophy (FSHD). In this study, we demonstrate that DUX4 induces expression of Krüppel-like factor 18 (KLF18), which is necessary for the subsequent activation of KLF17 and a subset of genes induced in the DUX4 transcriptional network.
Read the full summary ↓
Loss of KLF18 partially disrupts the DUX4 transcriptional network in both muscle cells and human embryonic stem cells, including genes associated with zygotic genome activation. KLF18 binds to the promoter regions of many of the genes it regulates but also requires DUX4 expression to transcriptionally activate many of its targets, indicating a feed-forward regulatory mechanism. While KLF17 and KLF18 have high homology in the zinc-finger DNA binding domain, human KLF18 contains a region with a variable number of tandem repeats (VNTRs) of fourteen amino acids predicted to form a beta-solenoid-like protein structure that is absent in rodent homologs and variably present in other species. Multiple structural variants consisting of different numbers and positions of repeat deletions are present in the human population, although initial studies do not show evidence of functional differences among the most common variants. These studies identify KLF18 as a key transcription factor in a feed-forward transcriptional network regulating early embryonic genes and the pathological DUX4 program in facioscapulohumeral dystrophy.
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 GSE299603_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: 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 PRJNA1275669 and SRA study SRP592087. Searching any of these in the dataset finder brings you back here.

Study design
3 × MB135 KLF17 vs 3 × MB135 KLF18 vs 3 × MB135 GFP

Supports a between-group comparison across 9 samples.

How we read this: 3 replicated groups read from 9 sample titles; they account for 9 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
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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.