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- W4320486578 abstract "Ferroptosis is an iron-dependent form of cell death driven by oxidation of polyunsaturated fatty acid (PUFA) phospholipids. Large-scale genetic screens have uncovered a specialized role for PUFA ether phospholipids (ePLs) in promoting ferroptosis. Understanding of the enzymes involved in PUFA-ePL production, however, remains incomplete. Here we show, using a combination of pathway mining of genetic dependency maps, AlphaFold-guided structure predictions and targeted lipidomics, that the uncharacterized transmembrane protein TMEM164—the genetic ablation of which has been shown to protect cells from ferroptosis—is a cysteine active center enzyme that selectively transfers C20:4 acyl chains from phosphatidylcholine to lyso-ePLs to produce PUFA ePLs. Genetic deletion of TMEM164 across a set of ferroptosis-sensitive cancer cell lines caused selective reductions in C20:4 ePLs with minimal effects on C20:4 diacyl PLs, and this lipid profile produced a variable range of protection from ferroptosis, supportive of an important but contextualized role for C20:4 ePLs in this form of cell death. The function of a poorly characterized transmembrane protein, TMEM164, was annotated by integrated genetic dependency mapping, AlphaFold2 structural modeling and lipidomics as an acyltransferase that generates ferroptotic C20:4 ether phospholipids." @default.
- W4320486578 created "2023-02-14" @default.
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- W4320486578 date "2023-02-13" @default.
- W4320486578 modified "2023-10-16" @default.
- W4320486578 title "TMEM164 is an acyltransferase that forms ferroptotic C20:4 ether phospholipids" @default.
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- W4320486578 doi "https://doi.org/10.1038/s41589-022-01253-7" @default.
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