Title : Triptolide suppresses IDH1-mutated malignancy via Nrf2-driven glutathione metabolism.

Pub. Date : 2020 May 5

PMID : 32312817






2 Functional Relationships(s)
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1 Our present study demonstrated that IDH1-mutated cells showed elevated levels of reactive oxygen species and higher demands on Nrf2-guided glutathione de novo synthesis. Reactive Oxygen Species isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens
2 Mechanistically, triptolide compromised the expression of GCLC, GCLM, and SLC7A11, which disrupted glutathione metabolism and established synthetic lethality with reactive oxygen species derived from IDH1 mutant neomorphic activity. Reactive Oxygen Species isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens