Preprint Data Descriptor Version 1 Preserved in Portico This version is not peer-reviewed

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

Version 1 : Received: 11 May 2023 / Approved: 12 May 2023 / Online: 12 May 2023 (14:47:52 CEST)

A peer-reviewed article of this Preprint also exists.

Kudryashova, O.M.; Nesterenko, A.M.; Korzhenevskii, D.A.; Sulyagin, V.K.; Tereshchuk, V.M.; Belousov, V.V.; Shokhina, A.G. Proteomic Shift in Mouse Embryonic Fibroblasts Pfa1 during Erastin, ML210, and BSO-Induced Ferroptosis. Data 2023, 8, 119. Kudryashova, O.M.; Nesterenko, A.M.; Korzhenevskii, D.A.; Sulyagin, V.K.; Tereshchuk, V.M.; Belousov, V.V.; Shokhina, A.G. Proteomic Shift in Mouse Embryonic Fibroblasts Pfa1 during Erastin, ML210, and BSO-Induced Ferroptosis. Data 2023, 8, 119.

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 was shown it's essential role in the pathogenesis in neurodegenerative diseases and an important role in therapy-resistant cancer cells. Thus, a detailed molecular understanding of both canonical and alternative ferroptosis pathways are 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 inactivate GPX4; L-buthionine sulfoximine (BSO) inhibits γ-glutamylcysteine synthetase, an essential enzyme for glutathione synthesis de novo. Most studies were focused on lipidomic profiling of model systems undergoing death in a ferroptotic modality.

Keywords

Ferroptosis; proteomics; LC-MS/MS; mouse embryonic fibroblasts; Pfa1; cell death; glutathione peroxidase 4; erastin; ML210; L-Buthionine-sulfoximine; BSO

Subject

Biology and Life Sciences, Biology and Biotechnology

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