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­­­Loss of Snhg5 disrupts cell-cycle regulation without altering cystogenesis in a mouse model of polycystic kidney disease.

GSE300255 Mus musculus (mouse) RNA-seq (gene expression) 10 samples Submitted 2025/06/30 Platform GPL34290
At a glance

RNA-seq (gene expression) · mouse · 10 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
10 samples: 4 × Wild-type mIMCD3 cells control WT vs 2 × Snhg5 null mIMCD3 cells KO vs 2 × Wild-type mouse kidney control WT vs 2 × Snhg5 null mouse kidney KOGroups 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
Loss of Snhg5 disrupts cell-cycle regulation without altering cystogenesis in a mouse model of polycystic kidney diseaseScientific reports · 2026
Summary (written by the submitters)
Long non-coding RNAs (lncRNAs) regulate diverse cellular pathways and are increasingly linked to human disease. Snhg5 is frequently described as a pathogenic lncRNA in many human diseases, including cancer. Our previous studies revealed that Snhg5 is one of the most upregulated lncRNAs in multiple mouse models of polycystic kidney disease (PKD).
Read the full summary ↓
Yet its role in renal biology and in autosomal dominant PKD (ADPKD) is not known. To elucidate the role of Snhg5, we generated a global Snhg5-null mouse. Homozygous animals were viable and displayed normal kidney morphology and function. RNA-sequencing of Snhg5-null kidneys and renal epithelial cells revealed common alterations in gene expression linked to cell cycle progression and DNA replication. At the molecular level, Snhg5-null cells showed an increased mitotic fraction, coinciding with depletion of ARPC5—a core ARP2/3 subunit— suggesting that reduced ARPC5 may contribute to this phenotype. To determine whether Snhg5 upregulation is pathogenic in mouse PKD, we crossed Snhg5-null mice with a collecting duct-specific Pkd1-mutant mouse model. Loss of Snhg5 did not attenuate cyst formation; if anything, disease severity was mildly but not significantly exacerbated. These findings indicate that Snhg5 modulates mitotic control and is dispensable for kidney development and cystogenesis in collecting duct-derived cysts.
Published in
Loss of Snhg5 disrupts cell-cycle regulation without altering cystogenesis in a mouse model of polycystic kidney disease
D'Amico S, Dar U, Eckberg K et al. · Scientific reports 2026 · PMID 41507385 · doi:10.1038/s41598-026-35234-w
This dataset
Open GSE300255 in finder → Find more mouse RNA-seq datasets →
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.

Series matrix ↓
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 GSE300255_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
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.

Raw reads on ENA ↗

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 PRJNA1279975 and SRA study SRP593352. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41507385) ↗
Study design
4 × Wild-type mIMCD3 cells control WT vs 2 × Snhg5 null mIMCD3 cells KO vs 2 × Wild-type mouse kidney control WT vs 2 × Snhg5 null mouse kidney KO

Supports a between-group comparison across 10 samples.

How we read this: 4 replicated groups read from 10 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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