Ten R M, Blank V, Le Bail O, Kourilsky P, Israël A
Unité de Biologie Moléculaire du Gène, INSERM U277, Institut Pasteur, Paris, France.
C R Acad Sci III. 1993;316(5):496-501.
The expression of class I genes of the Major Histocompatibility Complex is stimulated by IFN. The promoter of these genes contains an interferon response sequence (IRS) which overlaps the major enhancer. These elements are recognized by several protein factors, including IRF-1, which binds the IRS, and KBF1/NF-kappa B, which binds the enhancer. We demonstrate here that infection by Newcastle Disease Virus (NDV) results in an increased expression of class I genes, by a mechanism partially different from that of IFN, but that in both cases the cooperative action of IRF1 and KBF1/NF-kappa B is required. In F9 embryonal carcinoma cells, where KBF1/NF-kappa B activity cannot be detected, both types of stimuli are ineffective.
主要组织相容性复合体I类基因的表达受干扰素（IFN）刺激。这些基因的启动子包含一个与主要增强子重叠的干扰素反应序列（IRS）。这些元件可被几种蛋白质因子识别，包括与IRS结合的IRF-1以及与增强子结合的KBF1/NF-κB。我们在此证明，新城疫病毒（NDV）感染会导致I类基因表达增加，其机制部分不同于IFN，但在这两种情况下，都需要IRF1和KBF1/NF-κB的协同作用。在无法检测到KBF1/NF-κB活性的F9胚胎癌细胞中，这两种刺激均无效。
