The membrane-bound transcription factor CREB3L1 is activated in response to virus infection to inhibit proliferation of virus-infected cells.
The membrane-bound transcription factor CREB3L1 is activated in response to virus infection to inhibit proliferation of virus-infected cells.
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DOI：
10.1016/j.chom.2011.06.006
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发表时间：
2011-07-21
影响因子：
30.3
通讯作者：
Ye J
中科院分区：
文献类型：
--
作者：
Denard B;Seemann J;Chen Q;Gay A;Huang H;Chen Y;Ye J
CREB3L1/OASIS是一种细胞转录因子，作为膜结合的前体合成，在内质网应激等刺激下被调节的膜内蛋白分解激活。比较允许丙型肝炎病毒复制的Huh7亚克隆和不允许复制的亲本Huh7细胞的基因表达，我们确定CREB3L1是一种抑制病毒感染细胞增殖的细胞因子。当γ-疱疹病毒68、丙型肝炎病毒、西尼罗河病毒和仙台病毒等多种脱氧核糖核酸病毒感染后，CREB3L1被蛋白水解酶切割，使其NH2末端进入细胞核，诱导多个编码细胞周期抑制物的基因阻止细胞增殖。与此一致，我们观察到在含有丙型肝炎病毒或西尼罗河病毒复制子的增殖细胞中，有必要沉默CREB3L1的表达。我们的结果表明，CREB3L1可能通过抑制病毒感染细胞的增殖而在限制病毒传播方面发挥重要作用。
CREB3L1/OASIS is a cellular transcription factor synthesized as a membrane-bound precursor and activated by regulated intramembrane proteolysis in response to stimuli like ER stress. Comparing gene expression between Huh7 subclones that are permissive for hepatitis C virus (HCV) replication versus the non-permissive parental Huh7 cells, we identified CREB3L1 as a cellular factor that inhibits proliferation of virus-infected cells. Upon infection with diverse DNA and RNA viruses including murine γ-herpesvirus 68, HCV, West Nile virus (WNV) and Sendai virus, CREB3L1 was proteolytically cleaved, allowing its NH2-terminus to enter the nucleus to induce multiple genes encoding inhibitors of the cell cycle to block cell proliferation. Consistent with this, we observed a necessity for CREB3L1 expression to be silenced in proliferating cells that harbor replicons of HCV or WNV. Our results indicate that CREB3L1 may play an important role in limiting virus spread by inhibiting proliferation of virus-infected cells.
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