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题名: New perspectives for multi-level regulations of neuronal acetylcholinesterase by dioxins
作者: Xie, Heidi Q.; Xu, Tuan; Chen, Yangsheng; Li, Yunping; Xia, Yingjie; Xu, Sherry L.; Wang, Lingyun; Tsim, Karl W. K.; Zhao, Bin
刊名: CHEMICO-BIOLOGICAL INTERACTIONS
出版日期: 2016-11-25
卷号: 259, 期号:0, 页码:286-290
关键词: Dioxins ; Acetylcholinesterase ; MicroRNA ; Transcription ; Signaling pathway
DOI: 10.1016/j.cbi.2016.06.030
部门归属: 环境化学与生态毒理学国家重点实验室
英文摘要: Acetylcholinesterase (AChE; EC 3.1.1.7) is a vital functional enzyme in cholinergic neurotransmission which can rapidly hydrolyze neurotransmitter, acetylcholine, in the central and peripheral nervous systems. Emerging evidence showed that in addition to classical environmental AChE inhibitors, e.g. organophosphate and carbamate pesticides, dioxins are a new type of xenobiotic causing impairment of AChE. Dioxin can transcriptionally or post-transcriptionally suppress AChE expression in human neuroblastoma cells or mouse immune cells via the aryl hydrocarbon receptor (AhR) pathway, respectively. Dioxins can affect gene expression through other mechanisms, such as cross-talk with other signaling cascades and epigenetic modulations. Therefore, in this review, by summarizing the known mechanisms of AChE regulation and dioxin-induced gene alteration, potential signaling cascades and epigenetic mechanisms are proposed for dioxin-mediated AChE regulation. Mitogen activated protein (MAP) kinase, 30, 50-cyclic adenosine monophosphate (cAMP) and calcium-related singaling pathways, as well as potential epigenetic mechanisms, such as DNA methylation, and post-transcriptional regulation via microRNAs, including hsa-miR-132, hsa-miR-212 and hsa-miR-25-3p are discussed here. These proposed mechanisms may be invaluable not only to promote comprehensive understanding of the action mechanisms for dioxin, but to illustrate the molecular basis of dioxin-induced health impacts. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
收录类别: SCI
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内容类型: 期刊论文
URI标识: http://ir.rcees.ac.cn/handle/311016/35904
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