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Zuhra, K., Tom, C

Many are confined to a re-discussion of Nrf2 and HDAC inhibition, lacking integration with its biosynthetic origins and failing to synthesize the rapidly expanding body of evidence on novel and underappreciated mechanisms

We observed increased TF activity for AP-1 family members (e.g., JUN and FOS) as well as other TFs identified through differential footprint analysis in the bulk stage (e.g., NFKB1, CREB1, ATF2, EGR1) with continuous exposure to ART ( Figure 8C )

MITOL knockout in both HeLa and C2C12 cells resulted in reduced mitochondrial iron levels (Extended Data Fig

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