Research Topics
Species | Bin GotohSummaryAffiliation: University of Fukui Country: Japan Publications
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Detail Information
Publications
Inhibition of the gamma interferon response by a Sendai virus C protein mutant with no STAT1-binding abilityBin Gotoh
Microbiology Section, Department of Pathological Sciences, Faculty of Medical Sciences, University of Fukui, Shimoaizuki 23 3, Matsuoka cho, Yoshida gun, Fukui 910 1193, Japan
FEBS Lett 567:291-6. 2004..These results suggest that C protein has the STAT1-binding-independent anti-IFN-gamma mechanism, which targets processes after the STAT1 nuclear translocation event...
The C-terminal half-fragment of the Sendai virus C protein prevents the gamma-activated factor from binding to a gamma-activated sequence siteBin Gotoh
Department of Microbiology, Fukui Medical University School of Medicine, Shimoaizuki 23 3, Matsuoka cho, Yoshida gun, 910 1193, Fukui, Japan
Virology 316:29-40. 2003..These results suggest the possibility that the C protein prevents the gamma-activated factor from binding to GAS elements through its interaction with the STAT1 N-terminal domain...
The STAT2 activation process is a crucial target of Sendai virus C protein for the blockade of alpha interferon signalingBin Gotoh
Department of Microbiology, Fukui Medical University School of Medicine, Yoshida gun, Fukui 910 1193, Japan
J Virol 77:3360-70. 2003..Furthermore, expression of STAT1 enhanced the inhibitory effect of the C protein on STAT2 activation in U3A cells. The C protein thus appears to participate in the inhibitory process for STAT2 activation through the STAT1 interaction...
C and V proteins of Sendai virus target signaling pathways leading to IRF-3 activation for the negative regulation of interferon-beta productionTakayuki Komatsu
Microbiology Section, Department of Pathological Sciences, Faculty of Medical Sciences, University of Fukui, Yoshida-gun, Fukui, 910-1193, Japan
Virology 325:137-48. 2004..These results suggest that C, Y1, Y2, and V block signaling pathways leading to IRF-3 activation to downregulate IFN-beta production...
Bovine parainfluenza virus type 3 accessory proteins that suppress beta interferon productionTakayuki Komatsu
Microbiology Section, Department of Pathological Sciences, Faculty of Medical Sciences, University of Fukui, 23 3 Shimoaizuki, Matsuoka, Yoshida gun, Fukui 910 1193, Japan
Microbes Infect 9:954-62. 2007..These results demonstrate that the target of the respirovirus C protein is undoubtedly different from that of the V protein...
[Virus interference with the host interferon-induction system]Bin Gotoh
Tanpakushitsu Kakusan Koso 49:511-6. 2004
Paramyxovirus strategies for evading the interferon responseBin Gotoh
Department of Microbiology, Fukui Medical University School of Medicine, Shimoaizuki 23 3, Matsuoka cho, Yoshida gun, Fukui 910 1193, Japan
Rev Med Virol 12:337-57. 2002....
Sendai virus C protein impairs both phosphorylation and dephosphorylation processes of Stat1Takayuki Komatsu
Department of Microbiology, Fukui Medical University School of Medicine, Fukui 910-1193, Japan
FEBS Lett 511:139-44. 2002..Interestingly, the dephosphorylation process of pY-Stat1 was also impaired. These effects on both phosphorylation and dephosphorylation processes were attributable to the function of the C protein...
Sendai virus C protein plays a role in restricting PKR activation by limiting the generation of intracellular double-stranded RNAKenji Takeuchi
Division of Microbiology and Infectious Diseases, Department of Pathology, Shiga University of Medical Science, Seta, Otsu, Shiga 520 2192, Japan
J Virol 82:10102-10. 2008..Taken together, these results demonstrate that the SeV C protein limits generation of dsRNA, thereby keeping PKR inactive to maintain intracellular protein synthesis...
Suppression of interferon-related promoter activation by hepatitis C virus proteins expressed in cultured cellsAkira Hiramatsu
Department of Virology, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima 734-8551, Japan
Hiroshima J Med Sci 55:71-7. 2006..These results suggest that multiple HCV proteins have a function in suppression of the anti-viral effect by interferon and may indicate a novel role of E1 and NS4B proteins in interferon antagonism...
