Kamini Kaushal

Nov 14, 2024 | cell.com | Zhiyi Chen |Alex Inague |Kamini Kaushal |Gholamreza Fazeli |Tasneem Cheytan |Florencio Porto Freitas | +26 more

Keywordsferroptosiscancer metabolismseleniumselenocysteine metabolismcell deathneuroblastomaIntroductionFerroptosis is a non-apoptotic form of cell death characterized by the iron-dependent accumulation of phospholipid hydroperoxides, ultimately leading to membrane rupture and cell death.1 Due to its association with various pathological conditions, including cancer, neurodegeneration, and tissue damage,2 the mechanisms regulating ferroptosis have garnered increasing interest.

Jun 6, 2024 | biorxiv.org | Zhiyi Chen |Alex Inague |Gholamreza Fazeli |Kamini Kaushal

AbstractSelenocysteine (Sec) metabolism is crucial for cellular function and ferroptosis prevention and has traditionally been thought to begin with the uptake of the Sec carrier selenoprotein P (SELENOP). Following uptake, Sec released from SELENOP undergoes metabolisation via selenocysteine lyase (SCLY), producing selenide, a substrate used by selenophosphate synthetase 2 (SEPHS2), which provides the essential selenium donor - selenophosphate - for the biosynthesis of the selenocysteine tRNA.