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As TNF-ais a proinammatory molecule known to be induced by stimuli common in the lungs of patients with CF, such as bacterial LPS, the possibility of blocking these effects by a drug already in use for long-time treatment in CF is relevant, and indicates that other TNF-aregulated genes beside GSTT1 and GSTM1 might be affected by AZM

Given the hypothesis proposed regarding reduced glutathione biosynthesis around this timeframe within our study, conversion of excess GLY to other amino acids offers a plausible explanation

Inhibiting the keap1/nrf2 protein-protein interaction with protein-like polymers

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Under normal physiological states, -synuclein maintains a dynamic balance between membrane-bound multimers and soluble monomers, the latter typically adopting a natively unfolded conformation