کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9245500 | 1209948 | 2005 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Hepatitis C virus expression suppresses interferon signaling by degrading STAT1
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کلمات کلیدی
IRFISREISGF3Small interfering RNA - RNA تداخل کوچکsiRNA - siRNAinterferon - اینترفرونIFN - اینترفرون هاELISA - تست الیزاEnzyme-linked immunosorbent assay - تست الیزاinterferon-stimulated gene factor 3 - عامل ژن تحریک کننده اینترفرون 3interferon-stimulated response element - عنصر پاسخ تحریک شده توسط اینترفرونinterferon response factor - فاکتور پاسخ اینترفرونAntigen - پادگِن یا آنتیژن
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
Background & Aims: The molecular mechanisms by which hepatitis C virus (HCV) antagonizes the antiviral actions of interferon (IFN) have not been fully characterized. Specifically, how HCV proteins impact on IFN signaling components has yet to be elucidated. We used an HCV cell-based expression model to examine the interaction between HCV protein expression and host type I IFN signaling components in the Jak-STAT kinase pathway. Methods: Full-length HCV and HCV subgenomic constructs corresponding to structural and each of the nonstructural proteins were transiently transfected into Huh-T7 cells. HCV expression was monitored by an HCV core antigen enzyme-linked immunosorbent assay. STAT1, P-STAT1, and HCV protein expression was investigated with immunoprecipitation and Western blots. Results: Overexpression and small interfering RNA studies showed that STAT1 was indispensable for control of HCV expression. STAT1 and P-STAT1 expression were markedly reduced in HCV-transfected cells. Full-length HCV, HCV core/E1/E2, and NS3-4A were each associated with decreased STAT1 expression, which was attributable to proteasome-dependent degradation of STAT1. HCV core, but not HCV E1, E2, NS3, NS4, or NS5, bound to STAT1. STAT2 expression was not affected by HCV. Conclusions: HCV expression selectively degrades STAT1 and reduces P-STAT1 accumulation in the nucleus in a proteasome-dependent manner. HCV core protein binds STAT1, suggesting that this viral protein is associated with STAT1 degradation. STAT1 plays an indispensable role in innate antiviral immunity against HCV expression. In turn, HCV subverts the Jak-STAT kinase by selectively inducing STAT1 degradation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gastroenterology - Volume 128, Issue 4, April 2005, Pages 1034-1041
Journal: Gastroenterology - Volume 128, Issue 4, April 2005, Pages 1034-1041
نویسندگان
Wenyu Lin, Won Hyeok Choe, Yoichi Hiasa, Yoshitaka Kamegaya, Jason T. Blackard, Emmett V. Schmidt, Raymond T. Chung,