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Keywords {🔍}

cells, death, doi, cell, ferroptosis, figure, erastin, pubmed, google, scholar, erastininduced, ros, fer, pmc, system, cancer, article, free, lethal, iron, uptake, treated, mitochondrial, cystine, inhibition, genes, irondependent, small, apoptosis, effect, molecule, inhibitor, glutamate, compounds, data, production, oxidative, slca, observed, lipid, silencing, nox, results, rsl, calu, process, required, levels, viability, nonapoptotic,

Topics {✒️}

oncogenic-ras-harboring cancer cells voltage-dependent calcium channels oncogenic ras-selective lethal na+-independent cystine/glutamate antiporter cell-free dpph assay na+-independent [14c]-cystine uptake ras-mutant tumor cells double-membrane enclosed vesicles pmc beta search erastin-induced death involves iron-dependent enzymes functioning disulfide-linked heterodimer composed dna-damaging agent camptothecin iron-responsive hemerythrin domain octanol-water partition coefficient beta-amyloid precursor protein n-substituted cyclic moiety shrna-cell line combinations initiate iron-dependent ferroptosis unique iron-dependent form genotype-selective antitumor agents ice-cold uptake buffer cell death/cytostasis induced iron-catalyzed ros production hras-mutant bjelr cells ros-dependent ferroptotic mechanism potentiated erastin-induced death erastin-induced death triggers scavenge free radicals n-cyclohexyl moiety serving iron-export ferroxidase activity iron-regulated ubiquitin ligase supplemental experimental procedures prevent rsl-induced death erastin-induced oxidative death glutamate-induced cell death greater erastin-suppressing potency free radical scavengers cell free conditions ras-selective lethal supplementary materials included ras-mutant tumors erastin-induced cell death erastin-induced ferroptosis exhibits h2dcfda-sensitive ros production xc-cystine/glutamate antiporter prevent erastin-induced death mtdna-encoded transcript levels matched mtdna-wild-type experimental procedures analysis

Questions {❓}

• How does erastin inhibit system xc−?
• Ras superfamily GEFs and GAPs: validated and tractable targets for cancer therapy?

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