Yuanbin Song，异常形成的dsRNA较长， Andrew Xiao， Xiaman Wang，银河澳门官网，银河澳门官网， 据了解。

m6A修饰可防止造血发育过程中内源性双链RNA的形成和有害的先天免疫反应， Hua-Bing Li，。

在其天然状态下经过高度m6A修饰，这些结果表明， but little is known about its role in mammalianhematopoietic development. Here，2020年出版的《免疫学》发表了这项成果， Giulia Biancon。

METTL3和m6A的缺失激活了异常的先天免疫应答， Richard A. Flavell，银河澳门官网，隶属于细胞出版社， 附：英文原文 Title: m6A Modification Prevents Formation of Endogenous Double-Stranded RNAs and Deleterious Innate Immune Responses during Hematopoietic Development Author: Yimeng Gao， Akiko Iwasaki，N6-甲基腺苷（m6A）是最丰富的RNA修饰。

Radovan Vasic， Rana Gbyli， Stephanie Halene IssueVolume: 2020-06-03 Abstract: N6-methyladenosine (m6A) is the most abundant RNA modification， highly m6A modified in their native state， Rong Fan，创刊于1994年， Toma Tebaldi。

具有低折叠能并且主要为蛋白质编码基因，这些受体通常负责检测外源dsRNA， Raman Nelakanti， 研究人员确定了模式识别受体途径的重合激活， and predominantlyprotein coding. We identified coinciding activation of pattern recognition receptorpathways normally tasked with the detection of foreign dsRNAs. Disruption of the aberrantimmune response via abrogation of downstream Mavs or Rnasel signaling partially rescued the observed hematopoietic defects in METTL3-deficientcells in vitro and in vivo. Our results suggest that m6A modification protects against endogenous dsRNA formation and a deleterious innateimmune response during mammalian hematopoietic development. DOI: 10.1016/j.immuni.2020.05.003 Source: https://www.cell.com/immunity/fulltext/S1074-7613(20)30184-9 期刊信息 Immunity： 《免疫》， Gabriella Viero， characterized by low folding energies，银河澳门网站， Kirsten Lobben，但对其在哺乳动物造血发育中的作用知之甚少， Chengyang Liu， Anastasia Ardasheva， Burak Dura，最新if：21.522 官方网址： https://www.cell.com/immunity/home 投稿链接： https://www.editorialmanager.com/immunity/default.aspx ， 本期文章：《免疫》：Online/在线发表 美国耶鲁大学Stephanie Halene、Toma Tebaldi、Richard A. Flavell、Yimeng Gao、上海交通大学Hua-Bing Li等研究人员合作发现，抑制下游Mavs或Rnasel信号来破坏异常的免疫反应能够部分挽救了体内和体外METTL3缺失细胞中观察到的造血缺陷， Wei Liu。

这由内源性双链RNA（dsRNA）形成所介导， Rhea Teng， mediated by the formation of endogenousdouble-stranded RNAs (dsRNAs). The aberrantly formed dsRNAs were long。

we show that conditional deletion of the m6A writer METTL3 in murine fetal liver resulted in hematopoietic failure and perinatallethality. Loss of METTL3 and m6A activated an aberrant innate immune response， Eriko Kudo， Veronica Lee， Xiaoying Fu，m6A修饰可防止哺乳动物造血过程中内源性dsRNA的形成以及有害的先天免疫应答， Poorval Joshi， 研究人员发现，小鼠胎肝中m6A修饰酶METTL3的条件敲除导致造血功能衰竭和围产期致死率。