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ER-phagy and proteostasis defects create a pre-malignant injury state in Kras-mediated tumourigenesis (Spatial transcriptomics)

GSE274979 Mus musculus (mouse) Spatial transcriptomics 95 samples Submitted 2025/08/06 Platform GPL30172
At a glance

Spatial transcriptomics · mouse · 95 samples

What it is
Spatial transcriptomicsGene activity measured with its position in a tissue section.
Organism
Mus musculus (mouse)
Samples
95 samples: 5 conditions, mostly with about 28 replicates eachGroups 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)
Pancreatic acinar cells are surprisingly resistant to pre-malignant transformation by the mutant Kras oncogene. Here, reporter mice show that an early, transcriptionally-mediated effect of Kras activation is downregulation of ER-phagy. Subsequently, stochastic failure of ER-phagy correlates with pre-malignant transdifferentiation into acinar-ductal metaplasia (ADM).
Read the full summary ↓
Genetic perturbation of ER-phagy, combined with proteomics and transcriptomics, reveals endogenous injury, micro-inflammation and ADM across the acinar epithelium. Phenotypically, this occurs alongside intra-acinar formation of distinctive insoluble aggregates of ER proteins, including the injury marker REG3B. Mechanistically, REG3B is shown to bind to the ER-phagy receptor CCPG1 to facilitate degradation. Strikingly, spatial transcriptomics shows that oncogenic Kras also drives this cell state in a highly stochastic fashion, again characterised by protein aggregation, partial ductal identity, evidence of injury and propensity for ADM. Importantly, expression of insoluble mutant REG3B shows that protein aggregate formation directly engenders this state. Pancreatic cancer can thus arise from stochastic proteostatic defects that are both made probable by, and co-operate with, oncogenic Kras.
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 GSE274979_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: Spatial studies usually ship Space Ranger style folders (count matrix plus tissue images). Look for them among the supplementary files.

Also filed as BioProject PRJNA1148668 and SRA study SRP526731. Searching any of these in the dataset finder brings you back here.

Study design
5 conditions, mostly with about 28 replicates each
Pancreas, Acini_REG3, ×28 Pancreas, Acini_Proximal, ×23 Pancreas, Acini_Distal, ×19 Pancreas, ADM, ×18 Pancreas, ADM_REG3, ×7

Supports a between-group comparison across 95 samples.

How we read this: 5 replicated groups read from 95 sample titles; they account for 95 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

+ 55 more — browse all 95 samples with per-sample file links →

Datasets on a similar topic

Search all mouse RNA-seq datasets in GEO →

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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.