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kim,heejin
식물노화·수명연구단
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Posttranscriptional modulation of KCNQ2 gene expression by the miR-106b microRNA family

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dc.contributor.authorKim, Kwon-Woo-
dc.contributor.authorKim, Keetae-
dc.contributor.authorHee-Jin Kim-
dc.contributor.authorKim, Byeol-I-
dc.contributor.authorBaek, Myungin-
dc.contributor.authorSuh, Byung-Chang-
dc.date.accessioned2022-01-05T00:30:43Z-
dc.date.available2022-01-05T00:30:43Z-
dc.date.created2021-12-15-
dc.date.issued2021-11-23-
dc.identifier.issn0027-8424-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/11000-
dc.description.abstract© 2021 National Academy of Sciences. All rights reserved.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.-
dc.language영어-
dc.publisherNational Academy of Sciences-
dc.titlePosttranscriptional modulation of KCNQ2 gene expression by the miR-106b microRNA family-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000723039000008-
dc.identifier.scopusid2-s2.0-85120307235-
dc.identifier.rimsid76923-
dc.contributor.affiliatedAuthorHee-Jin Kim-
dc.identifier.doi10.1073/pnas.2110200118-
dc.identifier.bibliographicCitationProceedings of the National Academy of Sciences of the United States of America, v.118, no.47-
dc.relation.isPartOfProceedings of the National Academy of Sciences of the United States of America-
dc.citation.titleProceedings of the National Academy of Sciences of the United States of America-
dc.citation.volume118-
dc.citation.number47-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaScience & Technology - Other Topics-
dc.relation.journalWebOfScienceCategoryMultidisciplinary Sciences-
dc.subject.keywordPlusPOTASSIUM CHANNEL SUBUNITS-
dc.subject.keywordPlusEPILEPSY-ASSOCIATED KCNQ2-
dc.subject.keywordPlusSPLICE VARIANTS-
dc.subject.keywordPlusHUMAN BRAIN-
dc.subject.keywordPlusNEURONS-
dc.subject.keywordPlusEXCITABILITY-
dc.subject.keywordPlusSUPPRESSION-
dc.subject.keywordPlusMUTATION-
dc.subject.keywordPlusSITES-
dc.subject.keywordAuthorDevelopmental regulation-
dc.subject.keywordAuthorKCNQ2 protein-
dc.subject.keywordAuthorKCNQ2/3 K+ channel-
dc.subject.keywordAuthorMiR-106b family-
dc.subject.keywordAuthorMiRNA-
Appears in Collections:
Center for Plant Aging Research (식물 노화·수명 연구단) > 1. Journal Papers (저널논문)
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