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The SETD7–H3K4me1–APLNR Axis Couples Epigenetic Signaling to Orchestrate Endoderm Specification in Human Pluripotent Stem Cells

GSE309012 Homo sapiens (human) RNA-seq (gene expression) 18 samples Submitted 2026/01/01 Platform GPL20301
At a glance

RNA-seq (gene expression) · human · 18 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
18 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 differentiation of human pluripotent stem cells into definitive endoderm (DE), a pivotal event in embryonic development, remains incompletely elucidated with respect to its epigenetic control. Here, we identified SETD7, a histone H3K4 monomethyltransferase (H3K4me1), as dynamically upregulated during DE specification, with its expression correlating strongly with the key lineage marker SOX17.
Read the full summary ↓
Genetic knockdown of SETD7 impaired DE formation, as evidenced by reduced expression of DE markers and disruption of APLNR-mediated PI3K/AKT/mTOR signaling—a phenotypic defect recapitulated by pharmacological inhibition of APLNR. Mechanistically, SETD7 facilitates H3K4me1 deposition at enhancer regions of APLNR, thereby promoting its transcriptional activation. Our findings unveil an epigenetic-regulatory axis wherein SETD7-mediated enhancer priming drives APLNR expression, ultimately activating the PI3K/AKT/mTOR cascade to promote endodermal commitment. Through an integrated approach incorporating doxycycline-inducible SETD7 knockdown in hESCs, pathway-specific pharmacology, ChIP-qPCR, and 3D organoid modeling, we decipher the spatiotemporal regulatory network governed by SETD7 during DE specification. This study highlights the critical crosstalk between histone modification landscapes and signal transduction during cell fate determination and establishes a novel strategy for manipulating differentiation trajectories.
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 GSE309012_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 PRJNA1333718 and SRA study SRP628322. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 18 more — browse all 18 samples with per-sample file links →

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