A viral kinase mimics S6 kinase to enhance cell proliferation
A viral kinase mimics S6 kinase to enhance cell proliferation
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DOI：
10.1073/pnas.1600587113
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发表时间：
2016-07-12
影响因子：
11.1
通讯作者：
Damania, Blossom
中科院分区：
文献类型：
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作者：
Bhatt, Aadra Prashant;Wong, Jason P.;Damania, Blossom
病毒依靠宿主细胞制造子代病毒粒子的成分。为了减轻对宿主细胞蛋白质合成的不可分割的依赖，病毒可以通过多种机制调节蛋白质合成。我们报道了由卡波西肉瘤相关疱疹病毒（KSHV）的开放阅读框36 （ORF36）编码的病毒蛋白激酶（vPK）通过模仿细胞蛋白S6激酶（S6KB1）的功能来增强蛋白质合成。与S6KB1类似，vPK磷酸化核糖体S6蛋白并上调整体蛋白合成。vPK还能增强细胞增殖和非锚定生长。此外，我们报道vPK和S6KB1都能磷酸化6-磷酸果糖-2激酶/果糖- 2,6 -二磷酸酶2 (PFKFB2)，这两种激酶都能促进内皮毛细血管小管的形成。
Viruses depend upon the host cell for manufacturing components of progeny virions. To mitigate the inextricable dependence on host cell protein synthesis, viruses can modulate protein synthesis through a variety of mechanisms. We report that the viral protein kinase (vPK) encoded by open reading frame 36 (ORF36) of Kaposi's sarcoma-associated herpesvirus (KSHV) enhances protein synthesis by mimicking the function of the cellular protein S6 kinase (S6KB1). Similar to S6KB1, vPK phosphorylates the ribosomal S6 protein and up-regulates global protein synthesis. vPK also augments cellular proliferation and anchorage-independent growth. Furthermore, we report that both vPK and S6KB1 phosphorylate the enzyme 6-phosphofructo-2-kinase/fructose-2, 6-bisphosphatase 2 (PFKFB2) and that both kinases promote endothelial capillary tubule formation.