MiR-29b controls fetal mouse neurogenesis by regulating ICAT-mediated Wnt/beta-catenin signaling
DC Field | Value | Language |
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dc.contributor.author | Shin, J. | - |
dc.contributor.author | Shin, Y. | - |
dc.contributor.author | Oh, S-M | - |
dc.contributor.author | Yang, H. | - |
dc.contributor.author | Yu, W-J | - |
dc.contributor.author | Lee, J-P | - |
dc.contributor.author | Huh, S-O | - |
dc.contributor.author | Lee, S. H. | - |
dc.contributor.author | Suh, Y-H | - |
dc.contributor.author | Chung, S. | - |
dc.contributor.author | Kim, H-S | - |
dc.date.accessioned | 2021-09-05T04:22:44Z | - |
dc.date.available | 2021-09-05T04:22:44Z | - |
dc.date.created | 2021-06-15 | - |
dc.date.issued | 2014-10 | - |
dc.identifier.issn | 2041-4889 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/97156 | - |
dc.description.abstract | beta-Catenin has been widely implicated in the regulation of mammalian development and cellular homeostasis. However, the mechanisms by which Wnt/beta-catenin signaling components regulate physiological events during brain development remain undetermined. Inactivation of glycogen synthase kinase (GSK)-3 beta leads to beta-catenin accumulation in the nucleus, where it couples with T-cell factor (TCF), an association that is disrupted by ICAT (inhibitor of beta-catenin and T cell factor). In this study, we sought to determine whether regulation of ICAT by members of the microRNA-29 family plays a role during neurogenesis and whether deregulation of ICAT results in defective neurogenesis due to impaired beta-catenin-mediated signaling. We found that miR-29b, but not miR-29a or 29c, is significantly upregulated in three-dimensionally cultured neural stem cells (NSCs), whereas ICAT is reduced as aged. Treatment with a miR-29b reduced the reporter activity of a luciferase-ICAT 3'-UTR construct whereas a control (scrambled) miRNA oligonucleotide did not, indicating that miR-29b directly targets the 3'-UTR of ICAT. We also found that treatment with miR-29b diminished NSC self-renewal and proliferation, and controlled their fate, directing their differentiation along certain cell lineages. Furthermore, our in vivo results showed that inhibition of miR-29b by in utero electroporation induced a profound defect in corticogenesis during mouse development. Taken together, our results demonstrate that miR-29b plays a pivotal role in fetal mouse neurogenesis by regulating ICAT-mediated Wnt/beta-catenin signaling. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.subject | NEURAL STEM-CELLS | - |
dc.subject | BETA-CATENIN | - |
dc.subject | DIFFERENTIATION | - |
dc.subject | EXPRESSION | - |
dc.title | MiR-29b controls fetal mouse neurogenesis by regulating ICAT-mediated Wnt/beta-catenin signaling | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Chung, S. | - |
dc.identifier.doi | 10.1038/cddis.2014.439 | - |
dc.identifier.scopusid | 2-s2.0-84928017825 | - |
dc.identifier.wosid | 000344994000045 | - |
dc.identifier.bibliographicCitation | CELL DEATH & DISEASE, v.5 | - |
dc.relation.isPartOf | CELL DEATH & DISEASE | - |
dc.citation.title | CELL DEATH & DISEASE | - |
dc.citation.volume | 5 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | NEURAL STEM-CELLS | - |
dc.subject.keywordPlus | BETA-CATENIN | - |
dc.subject.keywordPlus | DIFFERENTIATION | - |
dc.subject.keywordPlus | EXPRESSION | - |
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