Transcriptional and chromatin regulation in interferon and innate antiviral gene expression.
Transcriptional and chromatin regulation in interferon and innate antiviral gene expression.
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DOI：
10.1016/j.cytogfr.2018.10.003
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发表时间：
2018-12
影响因子：
13
通讯作者：
Horvath CM
中科院分区：
文献类型：
--
作者：
Au-Yeung N;Horvath CM
为了应对病毒感染，细胞自主的、基于转录的抗病毒程序参与产生抗性，损害病原体复制，并在先天性和适应性免疫中警告专业细胞。这种双阶段抗病毒程序包括I型干扰素（IFN）的生产，然后对IFN信号的响应。病原体识别导致IRF和NFκB因子的激活，这些因子独立或共同发挥作用，以招募细胞共激活因子，重塑染色质、修饰组蛋白并激活靶基因位点的RNA聚合酶II（Pol II），包括充分表征的IFNβ增强体。在随后对IFN的反应中，受体介导的JAK-STAT信号级联反应指导称为ISGF 3的IRF 9-STAT 1-STAT 2转录因子复合物的组装，ISGF 3招募其自身的重塑因子、共激活因子和Pol II机制的队列以激活广泛的IFN刺激基因的转录。IFN和抗病毒基因调控网络的调节不仅对于驱动对感染的先天免疫应答是重要的，而且还可以告知以过度活跃和组成型IFN和IFN刺激基因（ISG）表达为特征的越来越多的慢性疾病的治疗。在这里，基因特异性和基因组范围内的调查，在IFN和ISGs的染色质景观与IRF和STAT依赖性调节Pol II转录平行讨论。
In response to virus infections, a cell autonomous, transcription-based antiviral program is engaged to create resistance, impair pathogen replication, and alert professional cells in innate and adaptive immunity. This dual phase antiviral program consists of type I interferon (IFN) production followed by the response to IFN signaling. Pathogen recognition leads to activation of IRF and NFκB factors that function independently and together to recruit cellular coactivators that remodel chromatin, modify histones and activate RNA polymerase II (Pol II) at target gene loci, including the well-characterized IFNβ enhanceosome. In the subsequent response to IFN, a receptor-mediated JAK-STAT signaling cascade directs the assembly of the IRF9-STAT1-STAT2 transcription factor complex called ISGF3, which recruits its own cohort of remodelers, coactivators, and Pol II machinery to activate transcription of a wide range of IFN-stimulated genes. Regulation of the IFN and antiviral gene regulatory networks is not only important for driving innate immune responses to infections, but also may inform treatment of a growing list of chronic diseases that are characterized by hyperactive and constitutive IFN and IFN-stimulated gene (ISG) expression. Here, gene-specific and genome-wide investigations of the chromatin landscape at IFN and ISGs is discussed in parallel with IRF- and STAT-dependent regulation of Pol II transcription.
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影响因子：
3.7
作者：
Génin P;Lin R;Hiscott J;Civas A
通讯作者：
Civas A
DOI：
10.3109/10409238.2011.630974
发表时间：
2012-03
影响因子：
6.5
作者：
Bruns AM;Horvath CM
通讯作者：
Horvath CM
DOI：
10.4161/jkst.23931
发表时间：
2013-07-01
期刊：
JAK-STAT
影响因子：
--
作者：
Au-Yeung N;Mandhana R;Horvath CM
通讯作者：
Horvath CM
DOI：
10.1073/pnas.0400567101
发表时间：
2004-06-29
影响因子：
11.1
作者：
Chang, HM;Paulson, M;Levy, DE
通讯作者：
Levy, DE
DOI：
10.1073/pnas.87.21.8555
发表时间：
1990-11-01
影响因子：
11.1
作者：
FU, XY;KESSLER, DS;DARNELL, JE
通讯作者：
DARNELL, JE