{"title":"RNA editing enzyme ADAR1 in human iPS cells","authors":"Shota Katayama","doi":"10.14800/SCTI.914","DOIUrl":null,"url":null,"abstract":"Adenosine deaminases acting on RNA (ADARs) are enzymes related in RNA editing that converts adenosine residues to inosine specifically in double-stranded RNAs. ADAR regulates mRNA stability and gene expression. ADAR1-Dicer complexes promote microRNA processing and RNA interference (RNAi) gene silencing. ADAR1 is highly expressed in human pluripotent stem cells. Recently, we observed that ADAR1-deficiency in human iPS cells promotes caspase3-mediated apoptotic cell death. On the other hand, ADAR1-deficiency did not alter cell morphology, alkaline phosphatase (AP) staining activities and the expression levels of pluripotent marker genes, indicating that ADAR1 is not required for maintenance of pluripotency. Further, ADAR1 deficient iPS cells did not change proliferation rate. Altogether, we demonstrated that ADAR1 is necessary for existence of human iPS cells.","PeriodicalId":90974,"journal":{"name":"Stem cell and translational investigation","volume":"97 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2015-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Stem cell and translational investigation","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14800/SCTI.914","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Adenosine deaminases acting on RNA (ADARs) are enzymes related in RNA editing that converts adenosine residues to inosine specifically in double-stranded RNAs. ADAR regulates mRNA stability and gene expression. ADAR1-Dicer complexes promote microRNA processing and RNA interference (RNAi) gene silencing. ADAR1 is highly expressed in human pluripotent stem cells. Recently, we observed that ADAR1-deficiency in human iPS cells promotes caspase3-mediated apoptotic cell death. On the other hand, ADAR1-deficiency did not alter cell morphology, alkaline phosphatase (AP) staining activities and the expression levels of pluripotent marker genes, indicating that ADAR1 is not required for maintenance of pluripotency. Further, ADAR1 deficient iPS cells did not change proliferation rate. Altogether, we demonstrated that ADAR1 is necessary for existence of human iPS cells.