JNK activation mediates the apoptosis of xCT-deficient cells

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...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2008-06, Vol.370 (4), p.584-588
Main Authors: Qiao, Hai-Xuan, Hao, Chan-Juan, Li, Yan, He, Xin, Chen, Ri-Sheng, Cui, Jie, Xu, Zhi-Heng, Li, Wei
Format: Article
Language:English
Subjects:
Amino Acid Transport System y+ - genetics
Animals
Apoptosis
Apoptosis - genetics
Caspase 3 - metabolism
Caspase 9 - metabolism
Cell Line
Cystine/glutamate transporter
Endoplasmic Reticulum - metabolism
ER stress
Eukaryotic Initiation Factor-2 - metabolism
JNK
JNK Mitogen-Activated Protein Kinases - metabolism
Melanocytes - metabolism
Melanocytes - physiology
Mice
Mice, Mutant Strains
Oxidative stress
Transcription Factor CHOP - metabolism
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Summary: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.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2008.03.134