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• W4384203483 abstract "Ferroptosis is a unique variety of non-apoptotic cell death, driven by massive lipid oxidation in an iron-dependent manner. Since ferroptosis was introduced as a concept in 2012, it has demonstrated its essential role in the pathogenesis in neurodegenerative diseases and an important role in therapy-resistant cancer cells. Thus, detailed molecular understanding of both canonical and alternative ferroptosis pathways is required. There is a set of widely used chemical agents to modulate ferroptosis using different pathway targets: erastin blocks cystine–glutamate antiporter, system xc-; ML210 directly inactivates GPX4; and L-buthionine sulfoximine (BSO) inhibits γ-glutamylcysteine synthetase, an essential enzyme for glutathione synthesis de novo. Most studies have focused on the lipidomic profiling of model systems undergoing death in a ferroptotic modality. In this study, we developed high-quality shotgun proteome sequencing during ferroptosis induction by three widely used chemical agents (erastin, ML210, and BSO) before and after 24 and 48 h of treatment. Chromato-mass spectra were registered in DDA mode and are suitable for further label-free quantification. Both processed and raw files are publicly available and could be a valuable dynamic proteome map for further ferroptosis investigation." @default.
• W4384203483 created "2023-07-14" @default.
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• W4384203483 date "2023-07-12" @default.
• W4384203483 modified "2023-09-25" @default.
• W4384203483 title "Proteomic Shift in Mouse Embryonic Fibroblasts Pfa1 during Erastin, ML210, and BSO-Induced Ferroptosis" @default.
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• W4384203483 doi "https://doi.org/10.3390/data8070119" @default.
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