作者
Zhiyi Chen,Alex Inague,Kamini Kaushal,Gholamreza Fazeli,Danny Schilling,Thamara N. Xavier da Silva,Ancély Ferreira dos Santos,Tasneem Cheytan,Florêncio Porto Freitas,Umut Yildiz,Lucas G. Viviani,Rodrigo S. Abreu e Lima,Mikaela P. Pinz,Isadora Medeiros,T. Iijima,Thiago Gerônimo Pires Alegria,Railmara Pereira da Silva,Larissa Regina Diniz,Simon Weinzweig,Judith Klein‐Seetharaman,Andreas Trumpp,Adriana Mañas,Robert J. Hondal,Christoph Bartenhagen,Matthias Fischer,Briana K. Shimada,Lucia A. Seale,Thilo Samson Chillon,Marietta Fabiano,Lutz Schomburg,Ulrich Schweizer,Luís Eduardo Soares Netto,Flávia Carla Meotti,Tobias P. Dick,Hamed Alborzinia,Sayuri Miyamoto,José Pedro Friedmann Angeli
摘要
Selenocysteine (Sec) metabolism is crucial for cellular function and ferroptosis prevention and begins with the uptake of the Sec carrier, selenoprotein P (SELENOP). Following uptake, Sec released from SELENOP is metabolized via selenocysteine lyase (SCLY), producing selenide, a substrate for selenophosphate synthetase 2 (SEPHS2), which provides the essential selenium donor, selenophosphate (H
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