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LncRNA SNHG26 facilitates inflammatory to proliferative state transition of keratinocyte progenitors during wound healing

GSE218430 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 17 samples Submitted 2024/08/26 Platform GPL28038Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 17 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
17 samples: 16 distinct titles, 1 of them repeatedGroups 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
The lncRNA SNHG26 drives the inflammatory-to-proliferative state transition of keratinocyte progenitor cells during wound healingNature communications · 2024
Summary (written by the submitters)
The epidermal stem cell transition from inflammation to proliferation is a crucial process in tissue repair. However, the molecular mechanism underlying this process is poorly understood. Combined with lncRNA expression profiling of human acute wounds and functional screening, we identified SNHG26 as a pivotal regulator of inflammatory to proliferative state transition of keratinocyte progenitor cells.
Read the full summary ↓
Snhg26-deficient mice showed impaired wound healing characterized by increased inflammatory response and decreased reepithelization in the wound. Consistently, single-cell transcriptomic analysis of the wound-edge tissue identified proliferative, migratory, and proinflammatory basal progenitors, which were dramatically changed in Snhg26 deficient mice. Mechanically, SNHG26 binds with ILF2 to relocate this transcription factor from the inflammatory gene loci (such as JUN) to the LAMB3 genomic loci. Collectively, this work identified a conserved lncRNA SNHG26 as a master regulator of epidermal stem cell state transition from inflammation to proliferation, highlighting the importance of lncRNAs in tissue repair and regeneration.
Published in
The lncRNA SNHG26 drives the inflammatory-to-proliferative state transition of keratinocyte progenitor cells during wound healing
Li D, Liu Z, Zhang L et al. · Nature communications 2024 · PMID 39366968 · doi:10.1038/s41467-024-52783-8
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 GSE218430_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 PRJNA903815 and SRA study SRP408928. Searching any of these in the dataset finder brings you back here.

Study design
16 distinct titles, 1 of them repeated
CHIP Ctr-ASO ×2

How we read this: Read from 17 sample titles: 16 distinct titles with little repetition. 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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