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Nevertheless, even in the absence of glucose, albumin increased pathogenicity of 101, and an efg1 / cph1 deletion mutant (Supplementary Fig

Metagenomic analysis indicated enrichment in oxidative phosphorylation, arachidonic acid, and tryptophan metabolic pathways, as well as numerous GH109 family enzymes involved in mucin degradation 73

In this pathway, p62 binds to Keap1 via its Keap1-interacting region (KIR) and recruits it to the autophagosome through the LC3-interacting region (LIR), leading to Keap1 degradation in autolysosomes [29]