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Due to the fact that ACTL6A did not regulate NRF2, we could reach the conclusion that ACTL6A functions in conjunction with NRF2 to regulate GCLC expression at the transcriptional level
It is becoming increasingly evident that mammalian cells can modulate patterns of protein expression in response to hydroperoxide stress, by activating redox-sensitive transcription factors such as Egr-1, NF- B and AP-1, G-proteins and by activating cellular kinases such as the mitogen-activated protein kinase (MAPK) family.18 This oxidative-dependent cellular signalling pathways alteration may frequently lead, with a still unknown mechanism, to hepatocyte apoptosis
Glutathione disulfide sensitizes hepatocytes to TNF-mediated cytotoxicity via IKK- S-glutathionylation: a potential mechanism underlying non-alcoholic fatty liver disease
doi: 10.1210/endo.133.6.8243312 42 ThorensB
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