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Hepatitis C virus core protein potentiates c-Jun N-terminal kinase activation through a signaling complex involving TRADD and TRAF2

Title
Hepatitis C virus core protein potentiates c-Jun N-terminal kinase activation through a signaling complex involving TRADD and TRAF2
Authors
Park K.-J.Choi S.-H.Koh M.S.Kim D.J.Yie S.W.Lee S.Y.Hwang S.B.
Ewha Authors
이수영
SCOPUS Author ID
이수영scopus
Issue Date
2001
Journal Title
Virus Research
ISSN
0168-1702JCR Link
Citation
vol. 74, no. 1-2, pp. 89 - 98
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
The hepatitis C virus (HCV) core protein is a multifunctional viral nucleocapsid protein. Previously, it has been demonstrated that the HCV core protein interacts with the cytoplasmic domain of tumor necrosis factor receptor 1 (TNFR1). Since the TNFR1 is engaged in stimulation of transcriptional factor NF-κB and AP-1 through activation of IκB kinase and c-Jun N-terminal kinase (JNK, or stress-activated protein kinase), respectively, we have examined whether the interaction between core protein and TNFR1 can modulate JNK. In this study, we demonstrate that the HCV core protein synergistically activates TNFα-induced JNK at a core concentration dependent manner in human embryonic kidney (HEK) 293 cells. HCV core-mediated synergism of JNK activation was also detected in stable cells expressing HCV core protein. Furthermore, we demonstrate that HCV core protein does not compete with TNF receptor-associated death domain (TRADD) for its interaction with the death domain of TNFR1. Our in vivo data show that HCV core and TRADD form a ternary complex with TNFR1. These findings suggest that the HCV core protein modulates TNFR1 signaling and may, thus, play a role in chronic infection of HCV patients. © 2001 Elsevier Science B.V.
DOI
10.1016/S0168-1702(00)00251-3
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자연과학대학 > 생명과학전공 > Journal papers
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