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For the in vitro experiments, silencing CA9 abrogated ATT-I-mediated Claudin-1, Occludin, GPX4 and SLC7A11 upregulation in Erastin-treated Caco-2 cells, indicating that CA9 is an indispensable mediator for ATT-I to restrain Erastin-induced ferroptosis in Caco-2 cells

The extent of this phenomenon is poorly documented in the scientific litterature

These simulations utilized the lowest-energy solution of the NMR-derived ensemble of the p53 TAD2 -FOXO4-DRI complexes as our starting geometry (see methods)

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UCSF ChimeraX: Tools for structure building and analysis