PINK1 deficiency sustains cell proliferation by reprogramming glucose metabolism through HIF1
出版年份 2014 全文链接
标题
PINK1 deficiency sustains cell proliferation by reprogramming glucose metabolism through HIF1
作者
关键词
-
出版物
Nature Communications
Volume 5, Issue 1, Pages -
出版商
Springer Nature
发表日期
2014-07-24
DOI
10.1038/ncomms5514
参考文献
相关参考文献
注意:仅列出部分参考文献,下载原文获取全部文献信息。- Loss of PINK1 Attenuates HIF-1 Induction by Preventing 4E-BP1-Dependent Switch in Protein Translation under Hypoxia
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- Time-Dependent Stabilization of Hypoxia Inducible Factor-1α by Different Intracellular Sources of Reactive Oxygen Species
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- γ-Glutamylcysteine detoxifies reactive oxygen species by acting as glutathione peroxidase-1 cofactor
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- Aerobic Glycolysis: Meeting the Metabolic Requirements of Cell Proliferation
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- Parkinson's disease mutations in PINK1 result in decreased Complex I activity and deficient synaptic function
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- Loss of PINK1 Function Promotes Mitophagy through Effects on Oxidative Stress and Mitochondrial Fission
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- The bioenergetic and antioxidant status of neurons is controlled by continuous degradation of a key glycolytic enzyme by APC/C–Cdh1
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- Silencing of PINK1 Expression Affects Mitochondrial DNA and Oxidative Phosphorylation in DOPAMINERGIC Cells
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