Báo cáo khoa học: "Ephrin-B2 expression critically influences Nipah virus infection independent of its cytoplasmic tail"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Ephrin-B2 expression critically influences Nipah virus infection independent of its cytoplasmic tail | Virology Journal BioMed Central Open Access Ephrin-B2 expression critically influences Nipah virus infection independent of its cytoplasmic tail Lena Thiel1 Sandra Diederich1 Stephanie Erbar1 Dennis Pfaff2 Hellmut G Augustin2 and Andrea Maisner 1 Address institute of Virology Philipps University of Marburg Marburg Germany and 2Joint Research Division Vascular Biology Medical Faculty Mannheim University of Heidelberg CBTM and German Cancer Research Center DKFZ Heidelberg Germany Email Lena Thiel - thiellen@ Sandra Diederich - Stephanie Erbar - Erbar@ Dennis Pfaff - Hellmut G Augustin - Andrea Maisner - maisner@ Corresponding author Published 24 December 2008 Received II December 2008 Accepted 24 December 2008 Virology Journal 2008 5 163 doi 1743-422X-5-163 This article is available from http content 5 1 163 2008 Thiel et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Cell entry and cell-to-cell spread of the highly pathogenic Nipah virus NiV requires binding of the NiV G protein to cellular ephrin receptors and subsequent NiV F-mediated fusion. Since expression levels of the main NiV entry receptor ephrin-B2 EB2 are highly regulated in vivo to fulfill the physiological functions in axon guidance and angiogenesis the goal of this study was to determine if changes in the EB2 expression influence NiV infection. Results Surprisingly transfection of increasing EB2 plasmid concentrations reduced cell-to-cell fusion both in cells expressing the NiV glycoproteins and in cells infected with NiV. This effect was attributed to the .

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