摘要
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.
原文 | 英語 |
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頁(從 - 到) | 7876-7881 |
頁數 | 6 |
期刊 | Proceedings of the National Academy of Sciences of the United States of America |
卷 | 113 |
發行號 | 28 |
DOIs | |
出版狀態 | 已發佈 - 7月 12 2016 |
對外發佈 | 是 |
ASJC Scopus subject areas
- 多學科