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Ninjurins 1 Regulate Hematopoietic Stem Cell Amplification Through Canonical WNT Signaling Independently of Plasma Membrane Rupture Activity

GSE330969 Homo sapiens (human) RNA-seq (gene expression) 16 samples Submitted 2026/07/02 Platform GPL30173
At a glance

RNA-seq (gene expression) · human · 16 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
Homo sapiens (human)
Samples
16 samples: 16 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)
Ninjurin-1 (NINJ1), a protein recently linked to plasma membrane rupture (PMR) during inflammasome activation, plays a well-established role in cell death. However, its function in hematopoiesis has remained unexplored. In this study, we identify a novel, PMR-independent role for Ninj1 in regulating hematopoiesis using zebrafish models.
Read the full summary ↓
Ninj1 deficiency resulted in significantly reduced neutrophil, erythrocyte, and hematopoietic stem/progenitor cell (HSPC) numbers, independently of its plasma membrane rupture (PMR) activity. Surprisingly, Ninj1 deficiency also alleviated neutrophilia and keratinocyte hyperproliferation in a chronic inflammation model, revealing a role beyond inflammasome-mediated cell death. To further investigate thisnoncanonical function, we identified PMR-deficient Ninj1 mutants (A56P and D50A). Expression of the A56P mutant rescued hematopoietic defects in Ninj1-deficient larvae, while the dominant-negative D50A mutant recapitulated the phenotypes of Ninj1 deficiency, confirming that Ninj1 regulates hematopoiesis independently of PMR. Furthermore, Ninj1 deficiency increased susceptibility to intracellular bacterial infection due to impaired neutrophil and macrophage recruitment, while overexpression of the A56P mutant enhanced immune cell recruitment and resistance to infection. Finally, we discovered that Ninj1 and Ninj2 cooperatively regulate the amplification of nascent hematopoietic stem cells (HSCs) from the hemogenic endothelium via canonical Wnt signaling. Importantly, this regulatory mechanism is conserved in human HSPCs, underscoring its evolutionary significance and translational potential. These findings position Ninjurins as critical regulators of HSC development and immune responses, with promising implications for enhancing HSC production in regenerative medicine and developing therapies for hematological and infectious diseases.
This dataset
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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 GSE330969_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 PRJNA1466307 and SRA study SRP700606. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
16 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 16 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
Datasets on a similar topic

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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.