Transcriptional regulation by STAT1 and STAT2 in the interferon JAK-STAT pathway.
Transcriptional regulation by STAT1 and STAT2 in the interferon JAK-STAT pathway.
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DOI：
10.4161/jkst.23931
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发表时间：
2013-07-01
期刊：
影响因子：
--
通讯作者：
Horvath CM
中科院分区：
文献类型：
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作者：
Au-Yeung N;Mandhana R;Horvath CM
STAT 1和STAT 2蛋白是I型和III型干扰素（IFN）信号传导的关键介质，并且是细胞抗病毒应答和适应性免疫的重要组分。它们与IFN调节因子9（IRF 9）结合形成异源三聚体转录因子复合物，称为ISGF 3。IFN-刺激基因（ISG）表达的调节已被用作JAK-STAT信号传导和哺乳动物转录调节的模型，但迄今为止主要在单基因水平上进行分析。虽然ISGF 3介导的基因调控的许多方面被认为是适用于几种ISG的共同特征，但也有许多关于非典型STAT 1或STAT 2信号传导事件的不同情况以及有助于基因特异性转录的协同调节因子的不同模式的报道。最近的全基因组研究已经开始揭示ISG调控的更完整的概况，朝着全基因组理解基因特异性行为的一般机制迈进。
STAT1 and STAT2 proteins are key mediators of type I and type III interferon (IFN) signaling, and are essential components of the cellular antiviral response and adaptive immunity. They associate with IFN regulatory factor 9 (IRF9) to form a heterotrimeric transcription factor complex known as ISGF3. The regulation of IFN-stimulated gene (ISG) expression has served as a model of JAK-STAT signaling and mammalian transcriptional regulation, but to date has primarily been analyzed at the single gene level. While many aspects of ISGF3-mediated gene regulation are thought to be common features applicable to several ISGs, there are also many reports of distinct cases of non-canonical STAT1 or STAT2 signaling events and distinct patterns of co-regulators that contribute to gene-specific transcription. Recent genome-wide studies have begun to uncover a more complete profile of ISG regulation, moving toward a genome-wide understanding of general mechanisms that underlie gene-specific behaviors.