MTERF2 contributes to MPP+-induced mitochondrial dysfunction and cell damage
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- 作者：Yanyan Hana ; 1 ; Peiye Gaoa ; 1 ; Shi Qiua ; Linbing Zhanga ; Ling Yanga ; Ji Zuoa ; Chunjiu Zhongb ; Shun Zhua ; shun_zhu@fudan.edu.cn" class="auth_mail" title="E-mail the corresponding author ; Wen Liua ; liuwen@shmu.edu.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：Mitochondrial transcription termination factors 2 (MTERF2) ; Mitochondrial dysfunction ; Parkinson's disease ; MPP+ ; Protein transport ; CCCP
- 刊名：Biochemical and Biophysical Research Communications
- 出版年：2016
- 出版时间：26 February 2016
- 年：2016
- 卷：471
- 期：1
- 页码：177-183
- 全文大小：1350 K
文摘
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The homeostasis of MTERF2 is crucial to the mitochondria and the cell.
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The expression levels of MTERF2 are elevated by MPP+ treatment in SH-SY5Y cells.
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The increased MTERF2 induced by MPP+ is mainly retained in the cytosolic fraction.
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MTERF2 knockdown alleviates MPP+-induced mitochondrial disruption and cell damage.