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Depletion of mitochondrial glutathione is thought to be one pathogenic factor in the development of alcoholic liver disease, and SAM, but not other glutathione prodrugs, prevents mitochondrial glutathione depletion in experimental alcoholic liver disease (possibly by protecting mitochondrial glutathione transport systems)

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These features enable LSM14 and EDC3 to function as standalone protein interaction platforms, instead of forming ringlike heptamers with RNAbinding interfaces

Wahid et al proposed the Bacteria may cause infection during the wound healing process, thereby affecting the healing process