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A viral kinase mimics S6 kinase to enhance cell proliferation.

Authors
  • Ap, Bhatt
  • Jp, Wong
  • Ms, Weinberg
  • Km, Host
  • Lc, Giffin
  • J, Buijnink
  • E, Van Dijk
  • Yoshihiro Izumiya
  • Hj, Kung
  • Br, Temple
  • B, Damania
Type
Published Article
Journal
Proceedings of the National Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Volume
113
Issue
28
Pages
7876–7876
Identifiers
DOI: 10.1073/pnas.1600587113
Source
Izumiya Lab dermatology-ucdavis
License
Unknown

Abstract

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.

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