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UGCG and the glycosphingolipid rheostat: a metabolic checkpoint governing immune activation and tumor immune evasion | Signal Transduction and Targeted Therapy

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Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Advertisement Signal Transduction and Targeted Therapy volume  10, Article number: 298 (2025) Cite this article 4177 Accesses 4 Citations 1 Altmetric Metrics details In a recent study in Cell, Morrison et al.1 identified Ugcg and B4galt5 as super-enhancer–driven genes essential for glycosphingolipid synthesis in natural killer (NK) cells and cytotoxic T cells. Genetic deletion or pharmacologic inhibition of UGCG disrupted cytotoxic granules, induced apoptosis, and blocked NK and CD8⁺ T cell expansion during viral infection, underscoring the critical role of glycosphingolipid metabolism in lymphocyte identity and effector

Download PDF Subjects Immunotherapy Translational immunology In a recent study in Cell , Morrison et al. 1 identified Ugcg and B4galt5 as super-enhancer–driven genes essential for glycosphingolipid synthesis in natural killer (NK) cells and cytotoxic T cells. Genetic deletion or pharmacologic inhibition of UGCG disrupted cytotoxic granules, induced apoptosis, and blocked NK and CD8⁺ T cell expansion during viral infection, underscoring the critical role of glycosphingolipid metabolism in lymphocyte identity and effector function. The human genome contains over one million enhancers, but only a

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