作为转录调节因子的干扰素诱导型p202蛋白：对核因子-κB、c-Fos和c-Jun活性的抑制作用
The interferon-inducible p202 protein as a modulator of transcription: inhibition of NF-kappa B, c-Fos, and c-Jun activities.
作者信息
Min W, Ghosh S, Lengyel P
机构信息
Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06520, USA.
出版信息
Mol Cell Biol. 1996 Jan;16(1):359-68. doi: 10.1128/MCB.16.1.359.
Abstract
The antimicrobial, immunomodulatory, and cell growth-regulatory activities of the interferons are mediated by interferon-inducible proteins. One of these is p202, a nuclear protein that is encoded by the Ifi 202 gene from the interferon-activatable gene 200 cluster. Overexpression of p202 in transfected cells slows down cell proliferation. As shown earlier, p202 binds to the hypophosphorylated form of the retinoblastoma susceptibility protein. Here we report that p202 inhibits the activities of the NF-kappa B and the AP-1 enhancers both in transiently transfected cells and in transfected stable cell lines overexpressing p202. Furthermore, p202 binds the NF-kappa B p50 and p65 and the AP-1 c-Fos and c-Jun transcription factors in vitro and in vivo. NF-kappa B, c-Fos, and c-Jun participate in the transcription of various cellular and viral genes, and thus p202 can modulate the expression of these genes in response to interferons.
摘要
干扰素的抗菌、免疫调节和细胞生长调节活性由干扰素诱导蛋白介导。其中之一是p202，一种核蛋白，由干扰素可激活基因200簇中的Ifi 202基因编码。p202在转染细胞中的过表达会减缓细胞增殖。如先前所示，p202与视网膜母细胞瘤易感蛋白的低磷酸化形式结合。在此我们报告，p202在瞬时转染细胞和过表达p202的转染稳定细胞系中均抑制NF-κB和AP-1增强子的活性。此外，p202在体外和体内均与NF-κB p50和p65以及AP-1 c-Fos和c-Jun转录因子结合。NF-κB、c-Fos和c-Jun参与各种细胞和病毒基因的转录，因此p202可以响应干扰素调节这些基因的表达。
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