突触发生
蛋白质组
生物
海马结构
蛋白质组学
突触可塑性
神经颗粒素
细胞生物学
基因表达
定量蛋白质组学
神经科学
基因
生物信息学
信号转导
生物化学
蛋白激酶C
受体
作者
Chen Yang,Mingming Zhang,Shuiming Li,Faping Yi,Haojun Huang,Hong Xie,Hangfei Liu,Rongzhong Huang,Jian Zhou
出处
期刊:Neuroscience
[Elsevier]
日期:2022-08-27
卷期号:503: 58-68
被引量:3
标识
DOI:10.1016/j.neuroscience.2022.08.019
摘要
Recent studies have demonstrated that Camk2b expression is modified in neuropsychiatric illnesses and potentially affects synaptic plasticity. However, the molecular events arising from Camk2b dysregulation are not fully elucidated and need to be comprehensively explored. In the present study, we first induced over-expression and under-expression of Camk2b in cultured rat hippocampal neurons through transfection with lentivirus plasmids. Then isobaric tag for relative and absolute quantitation (iTRAQ)-based quantitative proteomics followed by bioinformatics analyses were carried out to explore the impacts of Camk2b dysexpression on the proteome of the neurons. Compared with the respective controls, a total of 270 proteins in the Camk2b-overexpression group and 209 proteins in the Camk2b-underexpression group were experienced a divergence in expression. Gene ontology and pathway analyses indicated that Camk2b overexpression and under-expression respectively induced two different change profiles of protein expressions and functions, reflecting the potential differences in cellular processes and biological events. Through cross comparison, several candidate target proteins regulated directly by Camk2b were revealed. Further network and immunoblot analyses demonstrated that Mapk3 could be an important linker and Camk2b-Mapk3 might serve as a new potential pathway affecting the expression of synaptic proteins in hippocampal neurons. Collectively, the present results offer a new comprehension of the regulatory molecular mechanism of Camk2b and thereby increase our understanding of Camk2b-mediated synaptogenesis in synaptic plasticity.
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