ArticleResearch square2026
Unanchored ubiquitin chains promote the non-canonical inflammasome via UBXN1.
Article in Research square, 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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12 authors.
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Abstract
The non-canonical caspase-4 inflammasome is a crucial anti-bacterial immune mechanism, yet, when dysregulated, may contribute to sepsis pathogenesis. Its regulation is heavily reliant on transcriptional control of caspase-4 expression. However, posttranslational regulation of the caspase-4 inflammasome remains poorly understood. Here, we report that UBX domain-containing protein 1 (UBXN1) facilitates the non-canonical inflammasome via unanchored lysine 48- or 63-linked polyUb (K48/63-Ub) chains. UBXN1 deficiency impairs the LPS-induced caspase-4 inflammasome and pyroptosis, renders mice resistant to LPS and polymicrobial sepsis. Depleting cellular unanchored polyUb with ubiquitin-specific proteinase 5 (USP5) reduces, while inhibiting USP5 enhances, caspase-4 activation in a UBXN1-dependent manner.
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