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Induction of autophagy in axonal dystrophy and degeneration

In contrast, mutation of the C-terminal active site cysteine increases the activity of GLRX, presumably by preventing disulfide bond formation between the two active site cysteines 20,21 , and renders GLRX a monothiol enzyme only capable of catalysis of (de)glutathionylation 22

3 Additionally, they appear to modulate systemic inflammation via the gutadipose tissuebrain axis, with increased levels of beneficial microbes such as Akkermansia muciniphila and production of metabolites like inosine, which improve leptin sensitivity and reduce inflammation

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Pyroptosis in AML

doi: 10.3389/fcell.2018.00096