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Under these experimental conditions, GSH depletion with BSO inhibited the microbicidal activity of macrophages while its precursor NAC increased intracellular killing of mycobacteria also from human macrophages, which are normally not very effective in killing mycobacteria
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Under physiological conditions, α-synuclein aggregates are identified by autophagy adaptors like p62, incorporated into autophagosomes, and subsequently delivered to lysosomes for degradation by acid hydrolases, including cathepsins B and D
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