ArticleResearch square2026
GAPDH nuclear signaling regulates neutrophil migration and inflammatory skin responses.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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17 authors.
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Abstract
Neutrophils are the most abundant leukocytes and key regulators of tissue homeostasis and disease. Here we show that inhibiting Gapdh nuclear translocation limits neutrophil infiltration into inflamed skin, reduces their motility, and decreases keratinocyte hyperproliferation and cell death in a zebrafish model of skin inflammation. Wild-type Gapdh expression in neutrophils, but not a nuclear-translocation-deficient mutant, exacerbated inflammation. Pharmacological inhibition of GAPDH nuclear translocation also attenuated pathology-associated markers in human organotypic 3D skin models of inflammation. In psoriasis lesions, GAPDH levels were elevated with altered localization. Single-cell RNA-seq revealed that Gapdh nuclear translocation regulates a subset of inflammation-induced genes in neutrophils, including
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Registered trials
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