Characterization of beta-R1, a gene that is selectively induced by interferon beta (IFN-beta) compared with IFN-alpha
Characterization of beta-R1, a gene that is selectively induced by interferon beta (IFN-beta) compared with IFN-alpha
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DOI：
10.1074/jbc.271.37.22878
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发表时间：
1996-09-13
影响因子：
4.8
通讯作者：
Ransohoff, RM
中科院分区：
文献类型：
--
作者：
Rani, MRS;Foster, GR;Ransohoff, RM
我们报告的初步表征的基因命名β-R1，这是选择性表达的干扰素β（IFN-β）相比，IFN-α。在人星形细胞瘤细胞中，10 IU/mL IFN-β或2500 IU/mL IFN-α 2诱导β-R1达到同等程度。为了解决这种差异反应的机制，我们分析了诱导β-R1基因在纤维肉瘤细胞和衍生突变细胞缺乏所需的组件信号I型干扰素。在亲本2fTGH细胞系中，β-R1容易被IFN-β诱导，但不被重组IFN-α 2、IFN-α Con 1或IFN-α亚型的混合物诱导。IFN-α 8对β-R1的诱导作用较弱。在分别缺乏p48、STAT 1、JAK 1和STATE的突变细胞系U2 A、U3 A、U4 A和U6 A中，IFN-β不诱导β-R1。缺乏IFN-alpha和-beta受体的Ifnar 2.2组分的U 5A细胞也未能表达β-R1。U1 A细胞对IFN-β和IFN-α 8有部分应答，但缺乏β-R1表达，表明TYK 2蛋白对于诱导该基因是必需的。综上所述，这些结果表明，β-R1的表达在响应I型IFN需要IFN-刺激的基因因子3加上一个额外的组件，这是更有效地形成诱导IFN-β相比，IFN-α。
We report preliminary characterization of a gene designated beta-R1, which is selectively expressed in response to interferon beta (IFN-beta) compared with IFN-alpha. In human astrocytoma cells, beta-R1 was induced to an equivalent extent by 10 IU/mL IFN-beta or 2500 IU/mL IFN-alpha 2. To address the mechanism of this differential response, we analyzed induction of the beta-R1 gene in fibrosarcoma cells and derivative mutant cells lacking components required for signaling by type I IFNs. beta-R1 was readily induced by IFN-beta in the parental 2fTGH cell line, but not by recombinant IFN-alpha 2, IFN-alpha Con1, or a mixture of IFN-alpha subtypes. IFN-alpha 8 induced beta-R1 weakly. beta-R1 was not induced by IFN-beta in mutant cell lines U2A, U3A, U4A, and U6A, which lack, respectively, p48, STAT1, JAK1, and STATE. U5A cells, which lack the Ifnar 2.2 component of the IFN-alpha and -beta receptor, also failed to express beta-R1. U1A cells are partially responsive to IFN-beta and IFN-alpha 8 but lacked beta-R1 expression, indicating that TYK2 protein is essential for induction of this gene. Taken together, these results suggest that the expression of beta-R1 in response to type I IFN requires IFN-stimulated gene factor 3 plus an additional component, which is more efficiently formed on induction by IFN-beta compared with IFN-alpha.