JNK inhibition of VMAT2 contributes to rotenone-induced oxidative stress and dopamine neuron death-Reference-Cited by-同舟云学术

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JNK inhibition of VMAT2 contributes to rotenone-induced oxidative stress and dopamine neuron death

Published:2015-02 Issue: Volume:328 Page:75-81
ISSN:0300-483X
Container-title:Toxicology
language:en
Short-container-title:Toxicology

Author:

Choi Won-Seok,Kim Hyung-Wook,Xia Zhengui

Funder

National Research Foundation of Korea (NRF)

Ministry of Science, ICT & Future Planning

National Institutes of Health (NIH)

Publisher

Elsevier BV

Subject

Toxicology

Reference44 articles.

1. Expanding insights of mitochondrial dysfunction in Parkinson’s disease;Abou-Sleiman;Nat. Rev. Neurosci.,2006

2. Chronic systemic pesticide exposure reproduces features of Parkinson’s disease;Betarbet;Nat. Neurosci.,2000

3. D2/D3 receptor agonist ropinirole protects dopaminergic cell line against rotenone-induced apoptosis through inhibition of caspase- and JNK-dependent pathways;Chen;FEBS Lett.,2008

4. Two distinct mechanisms are involved in 6-hydroxydopamine- and MPP+-induced dopaminergic neuronal cell death: role of caspases, ROS, and JNK;Choi;J. Neurosci. Res.,1999

5. Mitochondrial complex I inhibition is not required for dopaminergic neuron death induced by rotenone, MPP+, or paraquat;Choi;Proc. Natl. Acad. Sci. U. S. A.,2008

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