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首页> 外文期刊>Molecular and Cellular Biology >Promyelocytic Leukemia Protein Isoform II Promotes Transcription Factor Recruitment To Activate Interferon Beta and Interferon-Responsive Gene Expression
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Promyelocytic Leukemia Protein Isoform II Promotes Transcription Factor Recruitment To Activate Interferon Beta and Interferon-Responsive Gene Expression

机译：早幼粒细胞白血病蛋白同工型II促进转录因子的募集，以激活干扰素β和干扰素响应基因的表达。

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To trigger type I interferon (IFN) responses, pattern recognition receptors activate signaling cascades that lead to transcription of IFN and IFN-stimulated genes (ISGs). The promyelocytic leukemia (PML) protein has been implicated in these responses, although its role has not been defined. Here, we show that PML isoform II (PML-II) is specifically required for efficient induction of IFN-β transcription and of numerous ISGs, acting at the point of transcriptional complex assembly on target gene promoters. PML-II associated with specific transcription factors NF-κB and STAT1, as well as the coactivator CREB-binding protein (CBP), to facilitate transcriptional complex formation. The absence of PML-II substantially reduced binding of these factors and IFN regulatory factor 3 (IRF3) to IFN-β or ISGs promoters and sharply reduced gene activation. The unique C-terminal domain of PML-II was essential for its activity, while the N-terminal RBCC motif common to all PML isoforms was dispensable. We propose a model in which PML-II contributes to the transcription of multiple genes via the association of its C-terminal domain with relevant transcription complexes, which promotes the stable assembly of these complexes at promoters/enhancers of target genes, and that in this way PML-II plays a significant role in the development of type I IFN responses.
机译：为了触发I型干扰素（IFN）反应，模式识别受体激活信号级联反应，从而导致IFN和IFN刺激基因（ISG）转录。尽管尚未定义其作用，但早幼粒细胞白血病（PML）蛋白已与这些反应有关。在这里，我们显示PML亚型II（PML-II）是有效诱导IFN-β转录和众多ISG所特有的，在目标基因启动子上的转录复合体装配点起作用。与特定转录因子NF-κB和STAT1以及共激活因子CREB结合蛋白（CBP）相关的PML-II有助于转录复合物的形成。没有PML-II会大大减少这些因子和IFN调节因子3（IRF3）与IFN-β或ISGs启动子的结合，并显着降低基因激活。 PML-II的独特C末端结构域对其活性至关重要，而所有PML异构体共有的N末端RBCC基序则是可有可无的。我们提出了一个模型，其中PML-II通过其C末端结构域与相关转录复合物的关联来促进多个基因的转录，从而促进这些复合物在靶基因的启动子/增强子上的稳定装配，并且在这种情况下PML-II在I型IFN反应发生中起重要作用。

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