复制酶翻译及复制转录复合体组装
中文名称
通路描述
进入和去包被后，SARS-CoV-1基因组RNA作为转录本，启动帽依赖的ORF1a翻译以产生多蛋白pp1a。ORF1a末端附近的滑动序列和RNA假结使约25-30%的核糖体发生-1移码，继续翻译ORF1b以产生更长的多蛋白pp1ab。pp1a和pp1ab的自切割产生15-16种非结构蛋白（nsps），具有各种功能。RNA依赖的RNA聚合酶（RdRP）活性由nsp12编码，而papain样蛋白酶（PLPro）和主要蛋白酶（Mpro）活性分别由nsp3和nsp5编码。nsp3、4和6诱导细胞膜重排形成双膜囊泡（DMVs），在此组装并锚定冠状病毒复制转录复合体（RTC）。程序性核糖体移码（PRF）可能由病毒或宿主因子调节，除了病毒RNA二级结构外。例如，PRRSV中nsp1蛋白通过潜在的RNA结合基序激活nsp1介导的PRF信号。宿主RNA结合蛋白ANXA2结合IBV基因组中的假结结构。早期分泌途径中的宿主因子似乎参与DMV形成和RTC组装：Golgi特异性 brefeldin A 抵抗鸟苷核苷酸交换因子1（GBF1）及其效应物ADP核糖基化因子1（ARF1）均对正常DMV形成和高效RNA复制至关重要，这是感染小鼠的甲型冠状病毒MHV的典型代表（Fung & Liu 2019）。
英文描述
FBXL7 down-regulates AURKA during mitotic entry and in early mitosis The protein levels of aurora kinase A (AURKA) during mitotic entry and in early mitosis can be reduced by the action of the SCF-FBXL7 E3 ubiquitin ligase complex consisting of SKP1, CUL1, RBX1 and FBXL7 subunits. FBXL7 is the substrate recognition subunit of the SCF-FBXL7 complex that associates with the centrosome-bound AURKA, promoting its ubiquitination and proteasome-mediated degradation. Overexpression of FBXL7 results in G2/M cell cycle arrest and apoptosis (Coon et al. 2011).FBXL7 protein levels are down-regulated by the action of the SCF-FBXL18 E3 ubiquitin ligase complex, consisting of SKP1, CUL1, RBX1 and the substrate recognition subunit FBXL18. FBXL18 binds to the FQ motif of FBXL7, targeting it for ubiquitination and proteasome-mediated degradation, counteracting its pro-apoptotic activity (Liu et al. 2015). Cell cycle stage-dependency of down-regulation of FBXL7 by FBXL18 is unknown.
所含基因
42 个基因