| Literature DB >> 27342859 |
Aadra Prashant Bhatt1, Jason P Wong1, Marc S Weinberg2, Kurtis M Host1, Louise C Giffin1, Joshua Buijnink3, Evert van Dijk3, Yoshihiro Izumiya4, Hsing-Jien Kung5, Brenda R S Temple6, Blossom Damania7.
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.Entities:
Keywords: KSHV; ORF36; S6K; cell signaling; viral protein kinase
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Year: 2016 PMID: 27342859 PMCID: PMC4948314 DOI: 10.1073/pnas.1600587113
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205