ArticleNature communications2026
Ninjurins regulate hematopoietic stem cell amplification through canonical WNT signaling independent of plasma membrane rupture.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- NINJ1: implications for plasma membrane rupture and disease.Biochemical Society transactions · 2026Review
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9 authors.
Funding
Abstract
Ninjurin-1 (NINJ1), a protein required for plasma membrane rupture (PMR) during inflammasome-mediated cell death, has no known role in hematopoiesis. Here, using zebrafish and human hematopoietic stem/progenitor cells (HSPCs), we identify an evolutionarily conserved, PMR-independent function of Ninjurins in HSPC development. Ninj1 deficiency reduced HSPC, neutrophil and erythrocyte numbers, whereas PMR-deficient Ninj1 mutants demonstrated that this function is independent of PMR. Ninj1 deficiency also impaired immune cell recruitment and increased susceptibility to bacterial infection. Mechanistically, Ninj1 and Ninj2 cooperatively promoted early HSPC amplification through canonical WNT signaling. Pharmacological and genetic activation of WNT signaling rescued hematopoietic defects in Ninjurin-deficient larvae, whereas inhibition of WNT abolished the effects of Ninj1 gain of function. Human CD34⁺ HSPCs showed reduced expansion and impaired WNT signaling following NINJ1/2 deficiency, demonstrating conservation of this pathway. These findings identify Ninjurins as regulators of HSPC expansion with potential applications in regenerative medicine.
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