Selenium Utilization by GPX4 Is Required to Prevent Hydroperoxide-Induced Ferroptosis.
By Irina Ingold, C. Berndt, Sabine Schmitt, S. Doll, G. Poschmann, Katalin Buday, A. Roveri, Xiaoxiao Peng, F. Freitas, Tobias Seibt and 14 more. Cell, 2017
1,457 citations recorded by the source corpus.
Subfields: Nutrition and Dietetics, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/926d9a57923a1a17c16873805d42df6f3b9f8c8a
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In Nutrition and Dietetics
In Pulmonary and Respiratory Medicine
Citations in the corpus
- CD8+ T cells and fatty acids orchestrate tumor ferroptosis and immunity via ACSL4 (2022, background): “Lysophosphatidylcholine acyltransferase 3 (LPCAT3) and lipoxygenases (LOX) are involved in the incorporation of arachidonyl-CoAs into phospholipids on membranes and oxidation of these phospholipids, respectively (Conrad and Pratt, 2019; Ingold et al., 2018; Wenzel et al., 2017).”
- Selenium, Selenoproteins, and Immunity (2018, background): “An essential role for one of these selenoproteins in the area of development was demonstrated by the recent study, which showed that GPX4 protects a critical population of interneurons from ferroptotic cell death [29].”
- Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications (2021, background): “GPx4 activity(175); it can also upregulate GPx4 expression through driving the transcriptional activators TFAP2c and Sp1, resulted in ferroptosis inhibition.(175)”
- Ferroptosis turns 10: Emerging mechanisms, physiological functions, and therapeutic applications. (2022, positive): “The replacement of the selenocysteine active site residue in GPX4 with cys in C57BL/ 6J 3 129S6SvEv mice affects, however, only specific interneurons in the brain, which Marcus Conrad and colleagues reported in 2018 (Ingold et al., 2018).”