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Proteomic Shift in Mouse Embryonic Fibroblasts Pfa1 during Erastin, ML210, and BSO-Induced Ferroptosis

Author

Listed:
  • Olga M. Kudryashova

    (Neurotechnology Laboratory, Federal Center of Brain Research and Neurotechnologies, Federal Medical Biological Agency, 117997 Moscow, Russia)

  • Alexey M. Nesterenko

    (Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Science, 117997 Moscow, Russia)

  • Dmitry A. Korzhenevskii

    (Neurotechnology Laboratory, Federal Center of Brain Research and Neurotechnologies, Federal Medical Biological Agency, 117997 Moscow, Russia)

  • Valeriy K. Sulyagin

    (Faculty of Biology, Lomonosov Moscow State University, 119234 Moscow, Russia)

  • Vasilisa M. Tereshchuk

    (Neurotechnology Laboratory, Federal Center of Brain Research and Neurotechnologies, Federal Medical Biological Agency, 117997 Moscow, Russia
    Institute of Translational Medicine, Pirogov Russian National Research Medical University, 117997 Moscow, Russia)

  • Vsevolod V. Belousov

    (Neurotechnology Laboratory, Federal Center of Brain Research and Neurotechnologies, Federal Medical Biological Agency, 117997 Moscow, Russia
    Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Science, 117997 Moscow, Russia)

  • Arina G. Shokhina

    (Neurotechnology Laboratory, Federal Center of Brain Research and Neurotechnologies, Federal Medical Biological Agency, 117997 Moscow, Russia
    Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Science, 117997 Moscow, Russia
    Institute of Translational Medicine, Pirogov Russian National Research Medical University, 117997 Moscow, Russia)

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.

Suggested Citation

  • Olga M. Kudryashova & Alexey M. Nesterenko & Dmitry A. Korzhenevskii & Valeriy K. Sulyagin & Vasilisa M. Tereshchuk & Vsevolod V. Belousov & Arina G. Shokhina, 2023. "Proteomic Shift in Mouse Embryonic Fibroblasts Pfa1 during Erastin, ML210, and BSO-Induced Ferroptosis," Data, MDPI, vol. 8(7), pages 1-7, July.
  • Handle: RePEc:gam:jdataj:v:8:y:2023:i:7:p:119-:d:1192614
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    References listed on IDEAS

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    1. Yilong Zou & Whitney S. Henry & Emily L. Ricq & Emily T. Graham & Vaishnavi V. Phadnis & Pema Maretich & Sateja Paradkar & Natalie Boehnke & Amy A. Deik & Ferenc Reinhardt & John K. Eaton & Bryan Ferg, 2020. "Plasticity of ether lipids promotes ferroptosis susceptibility and evasion," Nature, Nature, vol. 585(7826), pages 603-608, September.
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