Phosphorylation of tau at Y18, but not tau-fyn binding, is required for tau to modulate NMDA receptor-dependent excitotoxicity in primary neuronal culture
作者: Takashi MiyamotoLiana SteinReuben ThomasBiljana DjukicPraveen TanejaJoseph KnoxKeith VosselLennart Mucke
作者单位: 1Gladstone Institute of Neurological Disease
2University of California
3Gladstone Institutes
刊名: Molecular Neurodegeneration, 2017, Vol.12 (1)
来源数据库: Springer Journal
DOI: 10.1186/s13024-017-0176-x
关键词: CalciumExcitotoxicityFynNMDARsPhosphorylationTauY18
英文摘要: Hyperexcitability of neuronal networks can lead to excessive release of the excitatory neurotransmitter glutamate, which in turn can cause neuronal damage by overactivating NMDA-type glutamate receptors and related signaling pathways. This process (excitotoxicity) has been implicated in the pathogenesis of many neurological conditions, ranging from childhood epilepsies to stroke and neurodegenerative disorders such as Alzheimer’s disease (AD). Reducing neuronal levels of the microtubule-associated protein tau counteracts network hyperexcitability of diverse causes, but whether this strategy can also diminish downstream excitotoxicity is less clear.
原始语种摘要: Hyperexcitability of neuronal networks can lead to excessive release of the excitatory neurotransmitter glutamate, which in turn can cause neuronal damage by overactivating NMDA-type glutamate receptors and related signaling pathways. This process (excitotoxicity) has been implicated in the pathogenesis of many neurological conditions, ranging from childhood epilepsies to stroke and neurodegenerative disorders such as Alzheimer’s disease (AD). Reducing neuronal levels of the microtubule-associated protein tau counteracts network hyperexcitability of diverse causes, but whether this strategy can also diminish downstream excitotoxicity is less clear.
全文获取路径: Springer  (合作)
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来源刊物:
影响因子:4.007 (2012)

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关键词翻译
关键词翻译
  • neuronal 二乙基溴乙酰胺
  • modulate 
  • binding 装订
  • receptor 接受体
  • primary 一次的
  • dependent 从属的
  • excitatory 刺激性的
  • required 必需
  • protein 蛋白质
  • pathogenesis 发病机理