NLRP3 inflammasome is a crucial intracellular multiprotein complex for innate immunity.Its aberrant activation can cause a range of inflammatory and autoimmune diseases.Hence,precise regulation of its activation is essential for maintaining immune homeostasis.NLRP3 protein levels are a limiting step in inflammasome activation and must be controlled to avoid pathological damage and related diseases.Herein,ATP-induced NLRP3 inflammasome activation was significantly decreased in farnesyltransferase alpha(FNTA)knockdown-THP-1-derived macrophages.FNTA suppressed K48-linked ubiquitination of NLRP3 via its PRR motif,blocking NLRP3 recognition by the cargo receptor NDP52 and autophagic degradation and promoting NLRP3 inflammasome activation.
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