ArticleiScience2026
Downregulation of SPRED1 drives keratinocyte hyperproliferation in psoriasis via activation of the ERK-RSK1 signaling axis.
Article in iScience, 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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6 authors.
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Abstract
Psoriasis features excessive epidermal keratinocyte proliferation, and our previous work identified a non-synonymous mutation in SPRED1 in psoriasis, specifically an enrichment of c.A881T (p.Y294F) in exon 7 (chr15:38351210). Combining public database data and clinical skin specimens, this study confirmed reduced SPRED1 expression in psoriatic lesions. Functional investigations were performed using HaCaT/NHEK keratinocyte transfection models, imiquimod-induced psoriasis-like mouse models, pathway agonist/inhibitor rescue assays, co-immunoprecipitation and dual-luciferase detection. SPRED1 indirectly interacts with nuclear ERK to block ERK-RSK1 activation and restrain keratinocyte overgrowth, whereas miR-126 downregulates SPRED1 by direct targeting. Intradermal supplementation of recombinant SPRED1 alleviates skin pathological changes in mice. These findings define the miR-126/SPRED1/ERK-RSK1 regulatory cascade and support SPRED1 as a promising candidate target for psoriasis treatment.
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