Yuanyuan Hu, Qianwen Sun, Chen Zhang, Qingquan Sha, Xiulian Sun
{"title":"RE1沉默转录因子(REST)负调控染色体1q融合all1 (AF1q)基因的转录","authors":"Yuanyuan Hu, Qianwen Sun, Chen Zhang, Qingquan Sha, Xiulian Sun","doi":"10.1186/s12867-015-0043-7","DOIUrl":null,"url":null,"abstract":"<p>ALL1-fused from chromosome 1q (AF1q), originally considered as an oncogenic factor, has been implicated in neuronal development; however, its upstream regulatory mechanisms in neural system remained elusive.</p><p>Our study showed that REST (RE1 silencing transcription factor), a key transcription factor in neurodevelopment, could down-regulate the gene expression of <i>AF1q</i>. The promoter assay identified a neuron-restrictive silencer element at ?383 to ?363?bp of human <i>AF1q</i> promoter. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (CHIP) confirmed the binding of REST to the NRSE in <i>AF1q</i> gene promoter. Additionally, the negative correlation between the expression levels of <i>Af1q</i> and <i>Rest</i> in mice neurodevelopment supported the negative regulation of <i>AF1q</i> by REST and the potential functions of AF1q in neurodevelopment.</p><p>These results demonstrate that REST regulates <i>AF1q</i> gene transcription through directly binding to a NRSE at ?383 to ?363?bp of <i>AF1q</i> promoter.</p>","PeriodicalId":497,"journal":{"name":"BMC Molecular Biology","volume":"16 1","pages":""},"PeriodicalIF":2.9460,"publicationDate":"2015-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s12867-015-0043-7","citationCount":"3","resultStr":"{\"title\":\"RE1 silencing transcription factor (REST) negatively regulates ALL1-fused from chromosome 1q (AF1q) gene transcription\",\"authors\":\"Yuanyuan Hu, Qianwen Sun, Chen Zhang, Qingquan Sha, Xiulian Sun\",\"doi\":\"10.1186/s12867-015-0043-7\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>ALL1-fused from chromosome 1q (AF1q), originally considered as an oncogenic factor, has been implicated in neuronal development; however, its upstream regulatory mechanisms in neural system remained elusive.</p><p>Our study showed that REST (RE1 silencing transcription factor), a key transcription factor in neurodevelopment, could down-regulate the gene expression of <i>AF1q</i>. The promoter assay identified a neuron-restrictive silencer element at ?383 to ?363?bp of human <i>AF1q</i> promoter. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (CHIP) confirmed the binding of REST to the NRSE in <i>AF1q</i> gene promoter. Additionally, the negative correlation between the expression levels of <i>Af1q</i> and <i>Rest</i> in mice neurodevelopment supported the negative regulation of <i>AF1q</i> by REST and the potential functions of AF1q in neurodevelopment.</p><p>These results demonstrate that REST regulates <i>AF1q</i> gene transcription through directly binding to a NRSE at ?383 to ?363?bp of <i>AF1q</i> promoter.</p>\",\"PeriodicalId\":497,\"journal\":{\"name\":\"BMC Molecular Biology\",\"volume\":\"16 1\",\"pages\":\"\"},\"PeriodicalIF\":2.9460,\"publicationDate\":\"2015-09-05\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1186/s12867-015-0043-7\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"BMC Molecular Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://link.springer.com/article/10.1186/s12867-015-0043-7\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"BMC Molecular Biology","FirstCategoryId":"1085","ListUrlMain":"https://link.springer.com/article/10.1186/s12867-015-0043-7","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
ALL1-fused from chromosome 1q (AF1q), originally considered as an oncogenic factor, has been implicated in neuronal development; however, its upstream regulatory mechanisms in neural system remained elusive.
Our study showed that REST (RE1 silencing transcription factor), a key transcription factor in neurodevelopment, could down-regulate the gene expression of AF1q. The promoter assay identified a neuron-restrictive silencer element at ?383 to ?363?bp of human AF1q promoter. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (CHIP) confirmed the binding of REST to the NRSE in AF1q gene promoter. Additionally, the negative correlation between the expression levels of Af1q and Rest in mice neurodevelopment supported the negative regulation of AF1q by REST and the potential functions of AF1q in neurodevelopment.
These results demonstrate that REST regulates AF1q gene transcription through directly binding to a NRSE at ?383 to ?363?bp of AF1q promoter.
期刊介绍：
BMC Molecular Biology is an open access journal publishing original peer-reviewed research articles in all aspects of DNA and RNA in a cellular context, encompassing investigations of chromatin, replication, recombination, mutation, repair, transcription, translation and RNA processing and function.
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