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Further, these data suggest that at acute time points following Gclc genetic deletion, compensation by NRF1 could be responsible for the dispensable role of NRF2 in GSH-depleted conditions
[PubMed] Pierre S, Chevallier A, Teixeira-Clerc F, Ambolet-Camoit A, Bui LC, Bats AS, Fournet JC, Fernandez-Salguero P, Aggerbeck M, Lotersztajn S, Barouki R, Coumoul X (2014) Aryl hydrocarbon receptor-dependent induction of liver fibrosis by dioxin
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CG: Investigation, Writing original draft
Caporaso, J
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