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作 者:Yongqiang Wang Long Zhang Fangfang Zhou
机构地区:[1]Institutes of Biology and Medical Science,Soochow University,Suzhou 215123,China [2]MOE Laboratory of Biosystems Homeostasis and Protection and Innovation Center for Cell Signaling Network,Life Sciences Institute,Zhejiang University,Hangzhou 310058,China
出 处:《Cellular & Molecular Immunology》2022年第8期867-868,共2页中国免疫学杂志(英文版)
基 金:a special program from the Ministry of Science and Technology of China(2021YFA101000);the Chinese National Natural Science Funds(U20A20393,U20A201376,31925013,3212500161,82041009,31871405,31701234,81902947,82041009,31671457,31571460 and 91753139);the Jiangsu Provincial Distinguished Young Scholars Award(BK20180043);the Key Project of the University Natural Science Foundation of Jiangsu Province(19KJA550003);a project funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions and the Postgraduate Research&Practice Innovation Program of Jiangsu Province(KYCX17_2036).
摘 要:A recent study by Tsvetkov et al.was published in Science and proposed a novel form of copper-induced cell death.Tsvetkov et al.revealed that excess intracellular copper induces the aggregation of lipoylated dihydrolipoamide S-acetyltransferase(DLAT),which is associated with the mitochondrial tricarboxylic acid(TCA)cycle,resulting in proteotoxic stress and leading to a novel form of cell death termed cuproptosis[1].
关 键 词:COPPER AGGREGATION EXCESS
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