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β-catenin是一种癌基因,在人类诸多肿瘤中高表达。肝细胞癌(HCC)是人类最多发的恶性肿瘤之一,慢性乙型肝炎病毒(HBV)携带者HCC发病的概率比非携带者高出100倍以上。本文所报道的就是有关HBV-X蛋白(HBX)如何导致β-catenin上调的机制。研究发现,被HBX激活的ERK通过与GSK-3β的一个结合序列结合并磷酸化GSK-3β的43苏氨酸位点,从而启动GSK-3β使其SER9被p90RSK磷酸化,最终导致GSK-3β的失活以及β-catenin的上调。
β-catenin is an oncogene that is highly expressed in many human tumors. Hepatocellular carcinoma (HCC) is one of the most malignant tumors in human. The incidence of HCC in patients with chronic hepatitis B virus (HBV) is more than 100 times higher than that of non-carriers. What is reported in this paper is about how HBV-X protein (HBX) causes the upregulation of beta-catenin. It has been found that activation of HBX by ERK activates GSK-3β by binding to a binding sequence of GSK-3β and phosphorylating the 43 threonine site of GSK-3β to phosphorylate SER9 by p90RSK, eventually leading to GSK-3β Inactivation and up-regulation of β-catenin.