The selenoprotein GPX4 is essential for mouse development and protects from radiation and oxidative damage insults.

By Levi J. Yant, Qitao Ran, L. Rao, H. Van Remmen, T. Shibatani, Jason G. Belter, Lucia Motta, Arlan Richardson, Thomas A. Prolla. Free Radical Biology & Medicine, 2003

760 citations recorded by the source corpus.

Subfields: Nutrition and Dietetics, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/c7dcafedd9981eef1f0000c3c3b5e33a3d6e7e32

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Citations in the corpus

Mitochondrial Glutathione, a Key Survival Antioxidant (2009, background): “The critical role of Gpx4 is underscored by the fact that whereas Gpx1-knockout mice are fully viable, Gpx4knockout animals demonstrate embryonic lethality, and Gpx4þ= cell lines are markedly sensitive to inducers of oxidative stress, including g-irradiation, tert-butyl-hydroperoxide, and hydrogen p”
Redox compartmentalization in eukaryotic cells. (2008, background): “Cell lines derived from Gpx4 knockout mice (Gpx4+/−) showed an increased sensitivity to diquat-induced mitochondrial dysfunction and loss of the membrane potential [57], suggesting that both Gpx1 and Gpx4 in mitochondria have a protective role against oxidative stress.”
Peroxidation of polyunsaturated fatty acids by lipoxygenases drives ferroptosis (2016, background): “Gpx4-deleted mice do not survive past embryonic day 8, indicating that protection from ferroptosis is likely essential during normal mammalian development (13, 14).”
Glutathione Peroxidase-1 in Health and Disease: From Molecular Mechanisms to Therapeutic Opportunities (2011, neutral): “…membrane-associated hydroperoxides, it is the only subtype of mammalian GPxs for which the knockout is lethal (320), but the precise cause of the midgestational le-thality caused by GPx-4 deﬁciency (401) is unknown, and may be unrelated to the reduction of phospholipid hydroperoxides by GPx-4.”
The Development of the Concept of Ferroptosis (2018, neutral): “death induced by γ-irradiation and tert-butyl hydroperoxide [88,89].”
GPx4, Lipid Peroxidation, and Cell Death: Discoveries, Rediscoveries, and Open Issues (2017, positive): “This observation complies with the distinct phenotype obtained by individual gene silencing (80, 111, 112), where only that of GPx4 is indispensable (52, 125).”
Selenium, Selenoproteins, and Immunity (2018, background): “In fact, there have been four individual selenoprotein knockout mice in which gene ablation was shown to result in embryonic lethality: GPX4, TXNRD1 and 2, and Selenoprotein T (SELENOT) [32,51,55,56].”
Selenium Utilization by GPX4 Is Required to Prevent Hydroperoxide-Induced Ferroptosis. (2017, positive): “TAM injection caused loss of GPX4 expression in Gpx4 animals to some extent (a gene-dosage effect has been previously reported) (Friedmann Angeli et al., 2014; Yant et al., 2003), whereas expression of mutant GPX4”