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The genetic inactivation of the regulatory component in the rate-limiting step of GSH biosynthesis ( GCLM ) or the treatment with L-BSO further depleted endogenous GSH in both ADH5 and WT cells, denoting that the mechanism by which ADH5 contributes to GSH homeostasis is downstream GSH synthesis

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We found that adipose-specific deletion of Ssu72 alleviated HFD-induced obesity and insulin resistance in mice

As will I

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