To further characterize these interactions, we constructed a molecular interaction network (Figure 7C) revealed three functionally interconnected modules: ( Consistent with multi-omics findings, KEGG pathway analysis identified glutathione metabolism as the most significantly perturbed shared pathway (Figure 8A), exhibiting coordinated changes between upregulated antioxidant enzymes such as Gpx3 and Mgst1 alongside depleted glutathione derivatives, supporting redox imbalance as a key pathogenic feature
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The nuclear protein fraction was extracted, and the relative Dnmt and 5-mC hydroxylase Tet activities were calculated based on the ratio of the treatment group to the control group after the normalization to the amount of protein
As the main antioxidant in our body, glutathione captures groups of molecules (free radicals) that can damage our cells and even our DNA, transporting them to the liver where it renews itself and returns to its function
While CBP/p300 is a well-validated direct interaction partner of NRF2 with prominent functions at enhancers, we report that this interaction is not required for NRF2-dependent NSCLC cell growth, indicating that NRF2 can sustain sufficient transcriptional activity in the absence of CBP/p300 coactivation