ARF1 and GBF1 generate a PI4P-enriched environment supportive of hepatitis C virus replication.
ARF1 and GBF1 generate a PI4P-enriched environment supportive of hepatitis C virus replication.
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DOI：
10.1371/journal.pone.0032135
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Chung RT
中科院分区：
文献类型：
--
作者：
Zhang L;Hong Z;Lin W;Shao RX;Goto K;Hsu VW;Chung RT
磷脂酰肌醇4-磷酸（PI 4P）的细胞水平已被证明是在几种病毒的RNA复制过程中上调，包括HCV复制子模型。然而，在感染性HCV模型中是否需要PI 4P仍然未知。此外，还没有确定宿主转运机制是否被HCV感染期间PI 4P的产生所隔离。在这里，我们发现，PI 4P富集在HCV复制复合物时，Huh 7.5.1细胞感染JFH 1。HCV复制被抑制后，过表达的PI 4P磷酸酶Sac 1。还发现PI 4P激酶PI 4KIII β是HCV复制所需的。此外，囊泡转运蛋白ARF 1和GBF 1与PI 4KIII β共定位，并且都是HCV复制所需的。在真正的HCV感染期间，PI 4P在病毒复制中起着不可或缺的作用。
Cellular levels of phosphatidylinositol 4-phosphate (PI4P) have been shown to be upregulated during RNA replication of several viruses, including the HCV replicon model. However, whether PI4P is required in an infectious HCV model remains unknown. Moreover, it is not established whether the host transport machinery is sequestered by the generation of PI4P during HCV infection. Here we found that PI4P was enriched in HCV replication complexes when Huh7.5.1 cells were infected with JFH1. HCV replication was inhibited upon overexpression of the PI4P phosphatase Sac1. The PI4P kinase PI4KIIIβ was also found to be required for HCV replication. Moreover, the vesicular transport proteins ARF1 and GBF1 colocalized with PI4KIIIβ and were both required for HCV replication. During authentic HCV infection, PI4P plays an integral role in virus replication.
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影响因子：
46.9
作者：
Einav, Shirit;Gerber, Doron;Bryson, Paul D.;Sklan, Ella H.;Elazar, Menashe;Maerkl, Sebastian J.;Glenn, Jeffrey S.;Quake, Stephen R.
通讯作者：
Quake, Stephen R.
影响因子：
46.9
作者：
通讯作者：
--
影响因子：
5.4
作者：
Amako, Yutaka;Sarkeshik, Ali;Siddiqui, Aleem
通讯作者：
Siddiqui, Aleem
影响因子：
64.5
作者：
Knight, Zachary A.;Gonzalez, Beatriz;Shokat, Kevan M.
通讯作者：
Shokat, Kevan M.
DOI：
10.3350/kjhep.2010.16.3.263
发表时间：
2010-09
期刊：
The Korean journal of hepatology
影响因子：
--
作者：
Jang JY;Chung RT
通讯作者：
Chung RT