JNK activation mediates the apoptosis of xCT-deficient cells
Hai-Xuan Qiao1, Chan-Juan Hao, Yan Li
1Key Laboratory of Molecular and Developmental Biology, Institute of Genetics & Developmental Biology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing, China.
Abstract:
System X(c)(-) is an anionic amino acid transport system highly specific for cystine and glutamate. The underlying mechanism of cell death of cultured cells from the subtle gray (sut) mouse which contains an xCT null mutation remains elucidated. Our results show that the death of sut cells is likely caused by apoptosis mediated by c-Jun N-terminal kinase (JNK). The JNK activation triggers both a caspase-dependent (caspases-9 and -3) and an ER stress-mediated (eIF2 and CHOP) pathway to induce apoptosis. These findings suggest the possible pathways involved in the cell death of xCT-deficient cells.
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