Y. P. Kang

This study shows that glutathione (GSH) is essential for lipid abundance in adult tissues, particularly in the liver, by repressing NRF2.

This study uses a CRISPR screen to identify redox vulnerabilities in KEAP1/NRF2 mutant NSCLC, finding that SOD2 loss enhances the efficacy of β-Lapachone by disrupting mitochondrial function.

This study identifies a non-canonical role of glutamate-cysteine ligase in preventing glutamate accumulation and ferroptosis under cystine starvation.

This study shows PHGDH depletion in adult mice is tolerated, with normal liver and pancreatic function, but reduced PHGDH leads to altered lipid homeostasis in the liver.

This study shows NNT promotes NSCLC tumor growth by maintaining Fe-S protein function through NADPH production, preventing mitochondrial dysfunction and ROS accumulation.

The paper identifies CDO1 as a metabolic liability in NSCLC by showing its silencing promotes proliferation through cysteine metabolism disruption.