ArticleProceedings of the National Academy of Sciences of the United States of America2026
Calsyntenin-3 suppresses inflammation via inhibition of TLR N-glycosylation and membrane localization.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- Toll-like receptors in innate immunity and inflammation: from fundamental biology to clinic insights.Immunity & inflammation · 2026Review
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8 authors.
Funding
Abstract
Excessive innate immune activation drives uncontrolled inflammation and multiple inflammatory diseases. Proper N-glycosylation of membrane-associated Toll-like receptor 4 (TLR4) is essential for its trafficking to the cell membrane and subsequent innate activation, yet the mechanisms regulating this process remain poorly understood. Through a genome-wide CRISPR screening, we identify calsyntenin-3 (CLSTN3) as a potent suppressor of TLR4-triggered inflammation in macrophages. Mechanistically, CLSTN3 binds to the oligosaccharyltransferase (OST) subunit DDOST, inhibiting its interaction with the catalytic subunit STT3A and impairing OST complex assembly, which reduces N-glycosylation and membrane translocation of TLR4. Furthermore, CLSTN3 also suppresses membrane translocation and activation of other TLRs, including TLR3, TLR7 and TLR9. In addition,
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