ArticleiScience2026
UBE2M-mediated EGFR neddylation drives keratinocyte proliferation in psoriasis.
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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8 authors.
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Abstract
Basal keratinocytes (KCs) exhibit enhanced proliferative activity alongside severely impaired differentiation in psoriasis. Accumulating evidence has implicated dysregulation of the neddylation pathway in various human diseases; however, its role in psoriasis remains largely unexplored. In this study, we assessed global neddylation levels and the expression of neddylation-associated enzymes in both human psoriatic lesions and imiquimod (IMQ)-induced murine models of psoriasis. Our results revealed a significant upregulation of the E2-conjugating enzyme UBE2M in psoriatic lesions. UBE2M promotes psoriatic pathogenesis by enhancing keratinocyte proliferation and inflammatory responses. Both genetic and pharmacological inhibition of UBE2M suppressed psoriasis-like development
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