GPX4 is a selenocysteine-containing protein that plays an essential role in repairing peroxidised phospholipids. Its role in organismal homeostasis has been known for decades, and it has been reported to play a pivotal role in cell survival and mammalian embryonic development. In recent years, GPX4 has been associated with a cell death modality dubbed ferroptosis. The framing of this molecular pathway of cell death was essential for understanding the conditions that determine GPX4 dependency and ultimately to the process of lipid peroxidation. Since its discovery, ferroptosis has been gaining momentum as a promising target for yet-incurable diseases, including cancer and neurodegeneration. Given the current interest, in the present review, we provide newcomers in the field with an overview of the biology of GPX4 and cover some of its most recent discoveries.
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June 2022
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The pore-forming BCL-2 family proteins mediate mitochondrial poration to initiate apoptosis through protei–protein and protein–lipid interactions. Structural biology has been used to elucidate their mechanisms of activation, dimerization, and interaction with membranes, and AlphaFold, which relies solely on sequence information, can accurately predict the activated states, from Moldoveanu and colleagues, pages 35 to 47.
Review Article|
June 27 2022
GPX4: old lessons, new features
In Collection
Cell death and survival
Biochem Soc Trans (2022) 50 (3): 1205–1213.
Article history
Received:
May 03 2022
Revision Received:
June 02 2022
Accepted:
June 07 2022
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