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This indicates that OCSCs exploit the PPAR/NF-B signaling axis to skew macrophages toward a tumor-promoting M2 phenotype (51)

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

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