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Deubiquitination of active NLRP3 triggers ASC aggregation and the recruitment of precaspase-1, which leads to the formation of the NLRP3 inflammasome and the release of proinflammatory cytokines such as IL-1 and IL-18

The autophagy adaptor p62/SQSTM1, essential for targeting ubiquitinated substrates to autophagosomes, is mutated in ALS and FTD, where impaired p62 function results in aggregation-prone protein accumulation and neuronal toxicity