GSTpi expression mediates dopaminergic neuron sensitivity in experimental parkinsonism.

Smeyne M; Boyd J; Raviie-Shepherd KJiao YPond BBHatler MWolf RHenderson CSmeyne RJ

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GSTpi expression mediates dopaminergic neuron sensitivity in experimental parkinsonism.

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The cause of 95 of Parkinson's disease (PD) cases is unknown. It is hypothesized that PD arises from an interaction of free-radical-generating agents with an underlying genetic susceptibility to these compounds. Here we use the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of parkinsonism to examine the role of a dual function protein, GSTpi, in dopaminergic neuron death. GSTpi is the only GST family member expressed in substantia nigra neurons. GSTpi reduction by pharmacological blockade, RNA inhibition, and gene targeting increases sensitivity to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, suggesting that differential expression of GSTpi contributes to the sensitivity to xenobiotics in the substantia nigra and may influence the pathogenesis of reactive oxygen species-induced neurological disorders including PD.

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《Proceedings of the National Academy of Sciences of the United States of America》 |2007年第6期|1977-1982|共6页
作者
Smeyne M; Boyd J; Raviie-Shepherd KJiao YPond BBHatler MWolf RHenderson CSmeyne RJ;
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作者单位

Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. America;

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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种英语
中图分类自然科学总论;
关键词
Dopamine; Glutathione S-Transferase pi; Neurons; Parkinsonian Disorders; 多巴胺; 神经元;

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GSTpi expression mediates dopaminergic neuron sensitivity in experimental parkinsonism.

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