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Essential role of NONO-HOXA1-Wnt axis in cardiomyocyte differentiation [ChIP-seq]

GSE295270 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 15 samples Submitted 2025/12/21 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 15 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
15 samples: 5 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.
Paper
Essential role of NONO-HOXA1-Wnt axis in cardiomyocyte differentiationNature communications · 2026
Summary (written by the submitters)
NONO is recognized as a critical molecular scaffold involved in both transcriptional and posttranscriptional regulation. Mutations in NONO are frequently linked to congenital heart diseases (CHDs) in humans. However, the mechanisms by which NONO regulates cardiac development remain elusive. Here, we identified NONO as a pivotal dual-function regulator of cardiomyocyte differentiation in human induced pluripotent stem cells (hiPSCs).
Read the full summary ↓
NONO deficiency in hiPSCs results in a distinct defect in early cardiomyocyte differentiation. Mechanistically, NONO interacts with HOXA1 and regulates the dynamic expression of key genes during early cardiomyocyte differentiation. ChIP-seq analysis reveals that NONO loss reduces HOXA1 occupancy at target genes, compromising its transcriptional regulation. Additionally, NONO and HOXA1 cooperatively activate the Wnt signaling. Taken together, these findings establish the NONO-HOXA1-Wnt axis as a key molecular mechanism in cardiomyocyte differentiation and provid insights into the etiology of CHDs associated with NONO mutations.
Published in
Essential role of NONO-HOXA1-Wnt axis in cardiomyocyte differentiation
Feng Z, Gao Y, Gao H et al. · Nature communications 2026 · PMID 41580430 · doi:10.1038/s41467-026-68760-2
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 GSE295270_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 PRJNA1253979 and SRA study SRP580398. Searching any of these in the dataset finder brings you back here.

Study design
5 conditions, mostly in duplicate
NONO_ChIP_in_WT_Day2 ×2 HOXA1-HA_ChIP_in_WT_Day2 ×2 HOXA1-HA_ChIP_in_NONO-KO_Day2 ×2 Input_in_WT_Day2 ×2 Input_in_NONO-KO_Day2 ×2 H3K27AC_in_WT_Day ×1 First ChIP_in_WT_Day2 overexpressing HOXA1-HA ×1 ReChIP_in_WT_Day2 overexpressing HOXA1-HA ×1 +2 more

Supports a between-group comparison across 10 samples.

How we read this: 5 replicated groups read from 15 sample titles; they account for 10 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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