Clk1 deficiency promotes neuroinflammation and subsequent dopaminergic cell death through regulation of microglial metabolic reprogramming-Reference-Cited by-同舟云学术

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Clk1 deficiency promotes neuroinflammation and subsequent dopaminergic cell death through regulation of microglial metabolic reprogramming

Published:2017-02 Issue: Volume:60 Page:206-219
ISSN:0889-1591
Container-title:Brain, Behavior, and Immunity
language:en
Short-container-title:Brain, Behavior, and Immunity

Author:

Gu Ruinan,Zhang Fali,Chen Gang,Han Chaojun,Liu Jay,Ren Zhaoxiang,Zhu Yi,Waddington John L.,Zheng Long Tai,Zhen Xuechu

Publisher

Elsevier BV

Subject

Behavioral Neuroscience,Endocrine and Autonomic Systems,Immunology

Reference52 articles.

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2. Cytosolic phospholipase A2 plays a crucial role in ROS/NO signaling during microglial activation through the lipoxygenase pathway;Chuang;J. Neuroinflamm.,2015

3. Cancer metabolism and the Warburg effect: the role of HIF-1 and PI3K;Courtnay;Mol. Biol. Rep.,2015

4. Molecular pathways of neurodegeneration in Parkinson’s disease;Dawson;Science,2003

5. MAPK14/p38alpha-dependent modulation of glucose metabolism affects ROS levels and autophagy during starvation;Desideri;Autophagy,2014

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