Protein phosphatases and DNA tumor viruses: transformation through the back door?

M C Mumby, G Walter
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引用次数: 40

Abstract

Cellular transformation by many oncogenic viruses is mediated by alterations in signal transduction pathways that control normal growth and proliferation. Common targets for many transforming viruses are pathways regulated by protein phosphorylation. The biochemical control of proteins in these pathways is a dynamic process that is regulated by the relative activities of protein kinases and phosphatases. Although there are numerous examples of viral oncogenes that encode protein kinases (Hunter, 1991), until recently there has been no evidence linking altered phosphatase activity to transformation. In this review we describe a novel mechanism, utilized by small DNA tumor viruses, in which viral oncogenes bind to and regulate a cellular protein serine/threonine phosphatase. The currently available evidence indicates that alteration of phosphatase activity and subsequent changes in phosphorylation levels is an important step in transformation by these viruses.

蛋白磷酸酶和DNA肿瘤病毒:通过后门转化?
许多致癌病毒的细胞转化是由控制正常生长和增殖的信号转导途径的改变介导的。许多转化病毒的共同目标是由蛋白磷酸化调控的途径。这些途径中蛋白质的生化控制是一个动态过程,受蛋白激酶和磷酸酶的相对活性调控。虽然有许多病毒致癌基因编码蛋白激酶的例子(Hunter, 1991),但直到最近,还没有证据表明磷酸酶活性的改变与转化有关。在这篇综述中,我们描述了一种新的机制,利用小DNA肿瘤病毒,其中病毒致癌基因结合并调节细胞蛋白丝氨酸/苏氨酸磷酸酶。现有证据表明,磷酸酶活性的改变和随后磷酸化水平的变化是这些病毒转化的重要步骤。
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