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Multiple Mechanisms Contribute to Robust Type 1 Diabetes Protection in Nfkbid Overexpressing NOD mice

GSE315028 Mus musculus (mouse) RNA-seq (gene expression) 17 samples Submitted 2026/05/01 Platform GPL19057
At a glance

RNA-seq (gene expression) · mouse · 17 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
17 samples: 6 × Foxp3-GFP+ Treg, Nfkbid transgenic, vs 6 × Foxp3-GFP+ Treg, NOD Control, vs 5 × Foxp3-GFP+ Treg, Nfkbid KO,Groups 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
Multiple Mechanisms Contribute to Robust Type 1 Diabetes Protection in Nfkbid- Overexpressing NOD MiceDiabetes · 2026
Summary (written by the submitters)
Transgenic overexpression of Nfkbid in NOD mice causes robust type 1 diabetes protection associated with expansion of Tregs with increased suppressive capacity. Complementarily, Nfkbid ablation leads to decreased Treg numbers, decreased suppressive capacity and accelerated diabetes.The goal of this experiment was to further identify molecular mechanisms underlying strong protection and susceptibility from type 1 diabetes imbued by modifying Nfkbid expression.
Read the full summary ↓
mRNA sequencing analysis of Tregs from NOD mice with absent or overexpressed Nfkbid was performed. Differential gene expression was calculated and Ingenuity Pathway analyses showed enrichment of cellular replication pathways. Understanding the mechanisms underlying protection from Nfkbid overexpression may lead to novel therapeutic avenues.
Published in
Multiple Mechanisms Contribute to Robust Type 1 Diabetes Protection in Nfkbid- Overexpressing NOD Mice
Dwyer JR, Racine JJ, Chapman HD et al. · Diabetes 2026 · PMID 41860446 · doi:10.2337/db25-0956
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 GSE315028_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 PRJNA1394897 and SRA study SRP658375. Searching any of these in the dataset finder brings you back here.

Study design
6 × Foxp3-GFP+ Treg, Nfkbid transgenic, vs 6 × Foxp3-GFP+ Treg, NOD Control, vs 5 × Foxp3-GFP+ Treg, Nfkbid KO,

Supports a between-group comparison across 17 samples.

How we read this: 3 replicated groups read from 17 sample titles; they account for 17 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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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.