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Prophylactic inhibition of LATS1/2 prior to high-dose irradiation promotes the regeneration of the damaged intestinal epithelium through Yap-dependent and independent mechanisms

GSE326240 Mus musculus (mouse) RNA-seq (gene expression) 8 samples Submitted 2026/07/31 Platform GPL30172
At a glance

RNA-seq (gene expression) · mouse · 8 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
Mus musculus (mouse)
Samples
8 samples: 8 samples, each with a distinct title — no replicated groupsGroups 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)
Intestinal epithelial cells can respond to ionizing radiation (IR) injury through Yap-driven regenerative pathways that facilitate the regeneration and repopulation of the intestinal epithelium. Yap is a key effector of the Hippo signaling pathway but the impact of pharmacologic approaches manipulating Yap activity as a means of promoting intestinal IR response have not been thoroughly evaluated.
Read the full summary ↓
This study evaluated a selective and potent small-molecule inhibitor of Yap’s upstream negative regulators LATS1 and LATS2 (LATS1/2) on small intestinal radiation response in vitro and in vivo. Transient administration of this compound prior to IR facilitated in vitro radioprotection using mouse-derived enteroids as well as an in vivo radioprotective effect when systemically administered to mice prior to doses of IR that normally result in gastrointestinal acute radiation syndrome (GI-ARS). Transient systemic treatment with NCGC-023 before IR decreased DNA-damage, pre-mitotic apoptosis, and aberrant mitosis in the crypt epithelium. Mechanistically, Lats1/2 inhibition with NCGC-023 prompted gene expression changes characteristic of both Yap-dependent regenerative responses and Yap-independent metallothionine stress responses.
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 GSE326240_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 PRJNA1444190 and SRA study SRP687279. Searching any of these in the dataset finder brings you back here.

Study design
8 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 8 sample titles: 8 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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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.