气候变化领域集成服务门户(CCPortal): Posttranscriptional modulation of KCNQ2 gene expression by the miR-106b microRNA family

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DOI	10.1073/pnas.2110200118
	Posttranscriptional modulation of KCNQ2 gene expression by the miR-106b microRNA family
	Kim K.-W.; Kim K.; Kim H.-J.; Kim B.-I.; Baek M.; Suh B.-C.
发表日期	2021
ISSN	0027-8424
卷号	118 期号:47
英文摘要	MicroRNAs (miRNAs) have recently emerged as important regulators of ion channel expression. We show here that select miR-106b family members repress the expression of the KCNQ2 K+ channel protein by binding to the 30-untranslated region of KCNQ2 messenger RNA. During the first few weeks after birth, the expression of miR-106b family members rapidly decreases, whereas KCNQ2 protein level inversely increases. Overexpression of miR-106b mimics resulted in a reduction in KCNQ2 protein levels. Conversely, KCNQ2 levels were up-regulated in neurons transfected with antisense miRNA inhibitors. By constructing more specific and stable forms of miR-106b controlling systems, we further confirmed that overexpression of precursor-miR-106b-5p led to a decrease in KCNQ current density and an increase in firing frequency of hippocampal neurons, while tough decoy miR-106b-5p dramatically increased current density and decreased neuronal excitability. These results unmask a regulatory mechanism of KCNQ2 channel expression in early postnatal development and hint at a role for miR-106b up-regulation in the pathophysiology of epilepsy. © 2021 National Academy of Sciences. All rights reserved.
英文关键词	Developmental regulation; KCNQ2 protein; KCNQ2/3 K+ channel; MiR-106b family; MiRNA
语种	英语
scopus关键词	antisense oligonucleotide; ion channel; messenger RNA; microRNA; microRNA 106b; potassium channel KCNQ2; unclassified drug; KCNQ2 protein, human; Kcnq2 protein, mouse; messenger RNA; microRNA; MIRN106 microRNA, human; nerve protein; potassium channel KCNQ2; 3' untranslated region; animal cell; animal tissue; Article; controlled study; current density; epilepsy; firing rate; gene expression regulation; gene overexpression; genetic transfection; hippocampus; KCNQ2 gene; male; mouse; nerve cell; nerve cell excitability; nonhuman; pathophysiology; postnatal development; protein binding; protein expression; protein family; protein processing; rat; regulatory mechanism; upregulation; animal; C57BL mouse; genetics; HEK293 cell line; human; metabolism; Sprague Dawley rat; tumor cell line; Animals; Cell Line, Tumor; Gene Expression Regulation, Neoplastic; HEK293 Cells; Humans; KCNQ2 Potassium Channel; Mice; Mice, Inbred C57BL; MicroRNAs; Nerve Tissue Proteins; Neurons; Rats; Rats, Sprague-Dawley; RNA, Messenger; Up-Regulation
来源期刊	Proceedings of the National Academy of Sciences of the United States of America
文献类型	期刊论文
条目标识符	http://gcip.llas.ac.cn/handle/2XKMVOVA/250976
作者单位	Department of Brain and Cognitive Sciences, Daegu Gyeongbuk Institute of Science and Technology, Daegu, 42988, South Korea; Department of New Biology, Daegu Gyeongbuk Institute of Science and Technology, Daegu, 42988, South Korea; Center for Plant Aging Research, Institute for Basic Science, Daegu, 42988, South Korea
推荐引用方式 GB/T 7714	Kim K.-W.,Kim K.,Kim H.-J.,et al. Posttranscriptional modulation of KCNQ2 gene expression by the miR-106b microRNA family[J],2021,118(47).
APA	Kim K.-W.,Kim K.,Kim H.-J.,Kim B.-I.,Baek M.,&Suh B.-C..(2021).Posttranscriptional modulation of KCNQ2 gene expression by the miR-106b microRNA family.Proceedings of the National Academy of Sciences of the United States of America,118(47).
MLA	Kim K.-W.,et al."Posttranscriptional modulation of KCNQ2 gene expression by the miR-106b microRNA family".Proceedings of the National Academy of Sciences of the United States of America 118.47(2021).