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Your search keyword '"Ma, Chunmei"' showing total 8 results
Start Over Author "Ma, Chunmei" Journal brain research
8 results on '"Ma, Chunmei"'

4. miR-29c regulates BACE1 protein expression

Author

Zong, Yuanyuan, primary, Wang, Hailin, additional, Dong, Wei, additional, Quan, XiongZhi, additional, Zhu, Hua, additional, Xu, YanFeng, additional, Huang, Lan, additional, Ma, Chunmei, additional, and Qin, Chuan, additional

Published
2011
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6. Human mesenchymal stem cell transplantation protects against cerebral ischemic injury and upregulates interleukin-10 expression in Macaca fascicularis

Author

Li, Jiamei, primary, Zhu, Hua, additional, Liu, Ying, additional, Li, Qin, additional, Lu, Shan, additional, Feng, Ming, additional, Xu, Yanfeng, additional, Huang, Lan, additional, Ma, Chunmei, additional, An, Yihua, additional, Zhao, Robert Chunhua, additional, Wang, Renzhi, additional, and Qin, Chuan, additional

Published
2010
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8. G protein-coupled receptor kinase 5, overexpressed in the alpha-synuclein up-regulation model of Parkinson's disease, regulates bcl-2 expression.

Author

Liu P, Wang X, Gao N, Zhu H, Dai X, Xu Y, Ma C, Huang L, Liu Y, and Qin C

Subjects
Animals, Cell Line, Tumor, Cell Nucleus metabolism, Chromatin Immunoprecipitation methods, Cytoplasm metabolism, Disease Models, Animal, G-Protein-Coupled Receptor Kinase 5 genetics, Histone Deacetylases metabolism, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Neuroblastoma pathology, Parkinson Disease genetics, RNA, Small Interfering pharmacology, Transfection methods, Up-Regulation drug effects, Up-Regulation genetics, alpha-Synuclein genetics, G-Protein-Coupled Receptor Kinase 5 metabolism, Parkinson Disease metabolism, Proto-Oncogene Proteins c-bcl-2 metabolism, Up-Regulation physiology, alpha-Synuclein metabolism
Abstract

G protein-coupled receptor kinase 5 (GRK5) has been reported to accumulate in Lewy bodies (LBs), a histological hallmark of Parkinson's disease. Recent findings propose that GRK5 might function in Parkinson's disease via phosphorylation of alpha-synuclein, a major component of LBs. In this study, the changes of the expression levels of GRK5 and its possible effects in Parkinson's disease were evaluated in cell lines and transgenic mice model of alpha-synuclein overexpression. Both the expression levels of cytoplasmic and nuclear distributed GRK5 were induced an increase via alpha-synuclein overexpression in vivo and in vitro. The observations that the levels of alpha-synuclein phosphorylated at Ser-129 (pS129-alpha-synuclein) remain unchanged despite the downregulation of GRK5 by short hairpin ribonucleic acid (shRNA) transfection suggest that GRK5 is not the sole kinase involved in phosphorylating alpha-synuclein in Parkinson's disease. In addition, the findings that nuclear accumulation of GRK5 inhibits bcl-2 transcription and expression, at least in part by enhancing histone deacetylase (HDAC) activity, show an unexpected role for nuclear GRK5 in the regulation of an apoptosis-related gene. The present study suggests that GRK5 may be extensively involved in the mechanism of Parkinson's disease.

Published
2010
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