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Nrf2-Keap1 pathway promotes cell proliferation and diminishes ferroptosis

Kokaji, T

In conclusion, the available studies suggest that targeting glutamine metabolism can inhibit mitochondrial oxidative phosphorylation, reduce glutathione production, disrupt redox homeostasis, and inhibit mTORC1 activation in AML cells

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The disease is characterized by subnormal ALP levels and elevated PLP and phosphoethanolamine levels

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