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作 者:Chunxia Li Men Su Huimin Wang Yinghe Hu
机构地区:[1]Key Lab of Brain Functional Genomics,MOE&STCSM,Institute of Cognitive Neuroscience,East China Normal University [2]Shanghai Engineering Research Center for Molecular Therapeutics and New Drug Development,East China Normal University
出 处:《Neural Regeneration Research》2013年第29期2734-2743,共10页中国神经再生研究(英文版)
基 金:supported by the National Natural Science Foundationof China,No.30800312 and 30970368;the Specialized Research Fund for the Doctoral Program of Higher Education,No.20070269026;the Fundamental Research Fund for the Central Universities,No.78210020;Innovation Program of Shanghai Municipal Education Commission,No.10ZZ35
摘 要:NR2B subunits are involved in regulating aging, in particular, age-related learning and memory deficits. We examined 19-month-old NR2B transgenic mice and their littermate controls. First, we detected expression of the NR2B subunit gene, Grin2b, in the neocortex of transgenic mice using real-time PCR. Next, we used microarrays to examine differences in neocortical gene expression. Pathway and signal-net analyses identified multiple pathways altered in the transgenic mice, in-cluding the P53, Jak-STAT, Wnt, and Notch pathways, as well as regulation of the actin cytoskeleton and neuroactive ligand-receptor interactions. Further signal-net analysis highlighted the P53 and insulin-like growth factor pathways as key regulatory pathways. Our results provide new insight into understanding the molecular mechanisms of NR2B regulated age-related memory storage, normal organismal aging and age-related disease.NR2B subunits are involved in regulating aging, in particular, age-related learning and memory deficits. We examined 19-month-old NR2B transgenic mice and their littermate controls. First, we detected expression of the NR2B subunit gene, Grin2b, in the neocortex of transgenic mice using real-time PCR. Next, we used microarrays to examine differences in neocortical gene expression. Pathway and signal-net analyses identified multiple pathways altered in the transgenic mice, in-cluding the P53, Jak-STAT, Wnt, and Notch pathways, as well as regulation of the actin cytoskeleton and neuroactive ligand-receptor interactions. Further signal-net analysis highlighted the P53 and insulin-like growth factor pathways as key regulatory pathways. Our results provide new insight into understanding the molecular mechanisms of NR2B regulated age-related memory storage, normal organismal aging and age-related disease.
关 键 词:neural regeneration memorygrowth factor grants-supportedNR2B transgenic mice aging gene expression P53 insulin-likepaper NEUROREGENERATION
分 类 号:R338[医药卫生—人体生理学]
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