设为首页收藏本站

中国病毒学论坛|我们一直在坚持!

 找回密码
 立即注册

QQ登录

只需一步,快速开始

搜索
热搜: 活动 交友 discuz

Nat Immunol:重磅!曹雪涛院士课题组发现抗病毒免疫表观调控

查看数: 2873 | 评论数: 4 | 收藏 0
关灯 | 提示:支持键盘翻页<-左 右->
    组图打开中,请稍候......
发布时间: 2016-6-3 10:14

正文摘要:

      与原核生物不同,真核细胞的基因组DNA在细胞核里是以染色体形式存在的。在细胞生命活动过程中,包裹于染色体中的基因组DNA序列一般不发生改变,但细胞核内的染色体结构可以发生高度动态变 ...

回复

ipsvirus 发表于 2016-6-4 16:06:36
rojjer 发表于 2016-6-3 10:40
您最近什么对信号通路如此感兴趣!!!

免疫嘛  除了信号通路 还能做啥
序道 发表于 2016-6-3 10:51:57
研究太前沿了
rojjer 发表于 2016-6-3 10:40:49
您最近什么对信号通路如此感兴趣!!!
ipsvirus 发表于 2016-6-3 10:16:40
Methyltransferase Dnmt3a upregulates HDAC9 to deacetylate the kinase TBK1 for activation of antiviral innate immunity

Xia Li,        Qian Zhang, Yuanyuan Ding, Yiqi Liu, Dezhi Zhao, Kai Zhao, Qicong Shen, Xingguang Liu, Xuhui Zhu, Nan Li, Zhongyi Cheng, Guoping Fan, Qingqing Wang & Xuetao Cao

The DNA methyltransferase Dnmt3a has high expression in terminally differentiated macrophages; however, its role in innate immunity remains unknown. Here we report that deficiency in Dnmt3a selectively impaired the production of type I interferons triggered by pattern-recognition receptors (PRRs), but not that of the proinflammatory cytokines TNF and IL-6. Dnmt3a-deficient mice exhibited enhanced susceptibility to viral challenge. Dnmt3a did not directly regulate the transcription of genes encoding type I interferons; instead, it increased the production of type I interferons through an epigenetic mechanism by maintaining high expression of the histone deacetylase HDAC9. In turn, HDAC9 directly maintained the deacetylation status of the key PRR signaling molecule TBK1 and enhanced its kinase activity. Our data add mechanistic insight into the crosstalk between epigenetic modifications and post-translational modifications in the regulation of PRR signaling and activation of antiviral innate immune responses.

http://www.nature.com/ni/journal/vaop/ncurrent/full/ni.3464.html

QQ|论坛App下载|Archiver|小黑屋|中国病毒学论坛    

GMT+8, 2024-11-27 09:05 , Processed in 0.128340 second(s), 32 queries .

Powered by Discuz! X3.2

© 2001-2013 Comsenz Inc.

快速回复 返回顶部 返回列表