Giuseppe
Emeritus
J Virol. 2009 Jan 7. [Epub ahead of print]
The MAPK-activated kinase RSK2 plays a role in innate immune responses to influenza virus infection.
Kakugawa S, Shimojima M, Goto H, Horimoto T, Oshimori N, Neumann G, Yamamoto T, Kawaoka Y. - Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokaneda, Minato-ku, Tokyo 108-8639, Japan; Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Saitama 332-0012, Japan; Division of Oncology, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan; International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan; Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706, USA.
Viral infections induce signaling pathways in mammalian cells that stimulate innate immune responses and affect cellular processes, such as apoptosis, mitosis, and differentiation. Here, we report that the ribosomal protein S6 kinase alpha 3 (RSK2), which is activated through the 'classical' mitogen-activated protein kinase (MAPK) pathway, plays a role in innate immune responses to influenza virus infection.
RSK2 functions in the regulation of cell growth and differentiation, but was not known to play a role in cellular antiviral response.
We have found that knockdown of RSK2 enhanced the viral polymerase activity and growth of influenza viruses.
Influenza virus infection stimulates NK-kappaB- and IFN-beta-dependent promoters. This stimulation was reduced in RSK2 knockdown cells, suggesting that RSK2 executes its effect through innate immune response pathways.
Furthermore, RSK2 knockdown suppressed influenza virus-induced phosphorylation of the double-stranded RNA-activated protein kinase, PKR, a known antiviral protein. These findings establish a role for RSK2 in the cellular antiviral response.
PMID: 19129453 [PubMed - as supplied by publisher]
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The MAPK-activated kinase RSK2 plays a role in innate immune responses to influenza virus infection.
Kakugawa S, Shimojima M, Goto H, Horimoto T, Oshimori N, Neumann G, Yamamoto T, Kawaoka Y. - Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokaneda, Minato-ku, Tokyo 108-8639, Japan; Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Saitama 332-0012, Japan; Division of Oncology, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan; International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan; Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706, USA.
Viral infections induce signaling pathways in mammalian cells that stimulate innate immune responses and affect cellular processes, such as apoptosis, mitosis, and differentiation. Here, we report that the ribosomal protein S6 kinase alpha 3 (RSK2), which is activated through the 'classical' mitogen-activated protein kinase (MAPK) pathway, plays a role in innate immune responses to influenza virus infection.
RSK2 functions in the regulation of cell growth and differentiation, but was not known to play a role in cellular antiviral response.
We have found that knockdown of RSK2 enhanced the viral polymerase activity and growth of influenza viruses.
Influenza virus infection stimulates NK-kappaB- and IFN-beta-dependent promoters. This stimulation was reduced in RSK2 knockdown cells, suggesting that RSK2 executes its effect through innate immune response pathways.
Furthermore, RSK2 knockdown suppressed influenza virus-induced phosphorylation of the double-stranded RNA-activated protein kinase, PKR, a known antiviral protein. These findings establish a role for RSK2 in the cellular antiviral response.
PMID: 19129453 [PubMed - as supplied by publisher]
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