Identification of TRAIL as an interferon regulatory factor 3 transcriptional target
Identification of TRAIL as an interferon regulatory factor 3 transcriptional target
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DOI：
10.1128/jvi.79.14.9320-9324.2005
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发表时间：
2005-07-01
影响因子：
5.4
通讯作者：
Howley, PA
中科院分区：
文献类型：
--
作者：
Kirshner, JR;Karpova, AY;Howley, PA
病毒感染细胞中干扰素的产生和细胞凋亡是防止子代病毒产生和消除感染细胞所必需的。副粘病毒感染通过干扰素调节因子3（IRF-3）诱导细胞凋亡，但IRF-3如何发挥作用的确切机制尚不清楚。我们发现IRF-3参与了TRAIL的转录诱导，而TRAIL是凋亡途径中的关键参与者。IRF-3在病毒感染后上调TRAIL转录，并结合TRAIL启动子中的干扰素刺激的反应元件。病毒感染后，肿瘤坏死因子相关凋亡诱导配体及其受体DR 5的mRNA被诱导。这些研究将TRAIL鉴定为新的IRF-3转录靶点。
Interferon production and apoptosis in virus-infected cells are necessary to prevent progeny virus production and to eliminate infected cells. Paramyxovirus infection induces apoptosis through interferon regulatory factor 3 (IRF-3), but the exact mechanism of how IRF-3 functions is unknown. We show that IRF-3 is involved in the transcriptional induction of TRAIL, a key player in the apoptosis pathway. IRF-3 upregulates TRAIL transcription following viral infection and binds an interferon-stimulated response element in the TRAIL promoter. The mRNA for TRAIL and its receptor, DR5, are induced following viral infection. These studies identify TRAIL as a novel IRF-3 transcriptional target.