Modulation of hepatitis C virus RNA accumulation and translation by DDX6 and miR-122 are mediated by separate mechanisms.
Modulation of hepatitis C virus RNA accumulation and translation by DDX6 and miR-122 are mediated by separate mechanisms.
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DOI:
10.1371/journal.pone.0067437
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Wilson JA
中科院分区:
文献类型:
--
作者:
Huys A;Thibault PA;Wilson JA
DDX6 and other P-body proteins are required for efficient replication of Hepatitis C Virus (HCV) by unknown mechanisms. DDX6 has been implicated in miRNA induced gene silencing, and since efficient HCV replication and translation relies on the cellular microRNA, miR-122, we hypothesized that DDX6 had a role in the mechanism of action of miR-122. However, by using multiple HCV translation and replication assays we have found this is not the case. DDX6 silencing decreased HCV replication and translation, but did not affect the ability of miR-122 to stimulate HCV translation or promote HCV RNA accumulation. In addition, the negative effect of DDX6 silencing on HCV replication and translation was not dependent on miR-122 association with the HCV genome. Thus, DDX6 does not have a role in the activity of miR-122, and it appears that DDX6 and miR-122 modulate HCV through distinct pathways. This effect was seen in both Huh7.5 cells and in Hep3B cells, indicating that the effects are not cell type specific. Since infections by other viruses in the Flaviviridae family, including Dengue and West Nile Virus, also disrupt P-bodies and are regulated by DDX6, we speculate that DDX6 may have a common function that support the replication of several Flaviviruses.
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影响因子:
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作者:
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通讯作者:
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DOI:
10.1073/pnas.1012464108
发表时间:
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影响因子:
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发表时间:
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DOI:
10.1089/153685903321947996
发表时间:
2003-04-01
期刊:
HYBRIDOMA AND HYBRIDOMICS
影响因子:
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作者:
Eystathioy, T;Chan, EKL;Fritzler, MJ
通讯作者:
Fritzler, MJ