ArticleNature communications2026
p38α orchestrates BRAF
Article in Nature communications, 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.
The trial behind it
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding how tumor cells shape the tumor microenvironment (TME) and evade the host immune response is critical for developing novel therapeutic combinations. In this study, we identify tumor cell p38α as a therapeutic target that restricts antitumor immunity and contributes to resistance against immune-checkpoint inhibitors (ICIs). Genetic analyses of mouse and human melanomas reveal alterations in the mitogen-activated protein kinase (MAPK)-stress pathway, including upregulation of MAPK14. We demonstrate a dual role for p38α in ultraviolet-B (UVB)-induced Braf
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