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Neurochem Int 47: 92102 Waagepetersen HS, Sonnewald U, Larsson OM, Schousboe A
4 the drug molecules were bound well in the active site of the proteins
doi: 10.1097/01.asn.0000077404.45564.7e
Collectively, these observations establish that NRF2 alone can sustain sufficient transcriptional output to maintain cancer cell line growth and that metabolic reprogramming of cells driven by NRF2 does not require redox buffering via enhanced glutathione production
