《CDK5-LPL信號通路促進Aβ吞噬及其調控Tau蛋白磷酸化修飾研究》是紀建國為項目負責人,北京大學為依託單位的面上項目。
基本介紹
- 中文名:CDK5-LPL信號通路促進Aβ吞噬及其調控Tau蛋白磷酸化修飾研究
- 項目類別 :面上項目
- 依託單位 :北京大學
- 項目負責人:紀建國
科研成果 ,項目摘要,
科研成果
序號 | 標題 | 類型 | 作者 |
---|---|---|---|
1 | Deacetylation of TFEB promotes fibrillar A beta degradation by upregulating lysosomal biogenesis in microglia | 期刊論文 | Bao, Jintao(#); Zheng, Liangjun; Zhang, Qi; Li, Xinya; Zhang, Xuefei; Li, Zeyang; Bai, Xue; Zhang, Zhong; Huo, Wei; Wang, Qingsong; Ji, Jianguo; Zhao, Xuyang; Shang, Shujiang; Zhang, Chen; Wang, QS(*); Ji, JG(*); Zhang, C(*) |
2 | MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2. | 期刊論文 | Tang, L(#); Shen, H; Li, X; Li, Z; Liu, Z; Xu, J; Ma, S; Zhao, X; Bai, X; Li, M; Wang, Q; Ji, J(*) |
3 | PGC-1alpha/ERRalpha-Sirt3 Pathway Regulates DAergic Neuronal Death by Directly Deacetylating SOD2 and ATP Synthase beta. | 期刊論文 | Zhang, Xuefei(#); Ren, Xiaoqing; Zhang, Qi; Li, Zheyi; Ma, Shuaipeng; Bao, Jintao; Li, Zeyang; Bai, Xue; Zheng, Liangjun; Zhang, Zhong; Shang, Shujiang; Zhang, Chen; Wang, Chuangui; Cao, Liu; Wang, Qingsong; Ji, Jianguo(*) |
4 | 一種碳-13同位素標記的溴化膦化合物及製備方法和套用 | 專利 | 紀建國(#)(*); 王青松; 安明瑞 |
5 | Evaluation of the accuracy of protein quantification using isotope TMPP-labeled peptides. | 期刊論文 | Shen, Hongyan(#); An, Mingrui; Zou, Xiao; Zhao, Xuyang; Wang, Qingsong; Xing, Guowen; Ji, Jianguo(*) |
6 | Quantitative Phosphoproteomic Study Reveals that Protein Kinase A Regulates Neural Stem Cell Differentiation Through Phosphorylation of Catenin Beta-1 and Glycogen Synthase Kinase 3beta. | 期刊論文 | Wang, Shuxin(#); Li, Zheyi; Shen, Hongyan; Zhang, Zhong; Yin, Yuxin; Wang, Qingsong; Zhao, Xuyang; Ji, Jianguo(*) |
7 | Peroxiredoxin 6 Is a Crucial Factor in the Initial Step of Mitochondrial Clearance and Is Upstream of the PINK1-Parkin Pathway. | 期刊論文 | Ma, Shuaipeng(#); Zhang, Xuefei; Zheng, Liangjun; Li, Zeyang; Zhao, Xuyang; Lai, Wenjia; Shen, Hongyan; Lv, Junniao; Yang, Guofeng; Wang, Qingsong; Ji, Jianguo(*) |
8 | Quantitative proteomics reveals that PEA15 regulates astroglial A beta phagocytosis in an Alzheimer's disease mouse model | 期刊論文 | Lv, Junniao(#); Ma, Shuaipeng; Zhang, Xuefei; Zheng, Liangjun; Ma, Yuanhui; Zhao, Xuyang; Lai, Wenjia; Shen, Hongyan; Wang, Qingsong(*); Ji, Jianguo(*) |
9 | Quantitative Nuclear Proteomics Identifies that miR-137-mediated EZH2 Reduction Regulates Resveratrol-induced Apoptosis of Neuroblastoma Cells. | 期刊論文 | Ren, Xiaoqing(#); Bai, Xue; Zhang, Xuefei; Li, Zheyi; Tang, Lingfang; Zhao, Xuyang; Li, Zeyang; Ren, Yanfei; Wei, Shicheng; Wang, Qingsong(*); Liu, Cong(*); Ji, Jianguo(*) |
項目摘要
阿爾茨海默病(AD)嚴重危害人們的健康,其發病機制尚不清楚並缺乏有效的治療藥物。病理檢查發現腦組織中存在由Aβ澱粉樣蛋白組成的老年斑、神經炎性斑塊和Tau蛋白組成的神經纖維纏結等特徵,並在Aβ斑塊中發現脂蛋白、補體因子等蛋白以及在Aβ周圍活化的小膠質細胞。小膠質細胞在Aβ吞噬和清除過程中起了關鍵的作用。我們前期研究中首次發現細胞周期依賴激酶CDK5的調節亞基p25和脂蛋白酶LPL在Aβ吞噬過程中上調,導致CDK5活性升高,增強小膠質細胞吞噬Aβ的能力,但CDK5在Aβ吞噬與Tau蛋白過度磷酸化交叉調控作用機制研究未見報導。本課題擬利用細胞、轉基因動物模型、臨床樣本、高通量質譜技術平台,針對Aβ吞噬、CDK5調控的磷酸化修飾,系統研究小膠質細胞在Aβ吞噬過程中蛋白質的動態變化、CDK5功能及其調控Tau蛋白磷酸化修飾的信號網路,發現新的調控靶標和作用機制,為AD發病機制和治療提供新的依據。