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To respond to the high and dynamic NAD + cellular demand for both redox and nonredox processes, mammalian cells must synthesize NAD + from different dietary precursors through the de novo pathway and the PreissHandler pathway (Fig

Characterization of mammalian sulfiredoxin and its reactivation of hyperoxidized peroxiredoxin through reduction of cysteine sulfinic acid in the active site to cysteine

Arthroscopy 33(5):1026-1027, 2017

Wang and Chen, 2014), which results in the repression of GL2 (Serna and Martin, 2006

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