TAILIEUCHUNG - Báo cáo y học: " Nuclear Factor 90, a cellular dsRNA binding protein inhibits the HIV Rev-export function"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: " Nuclear Factor 90, a cellular dsRNA binding protein inhibits the HIV Rev-export function. | Retrovirology BioMed Central Open Access Nuclear Factor 90 a cellular dsRNA binding protein inhibits the HIV Rev-export function Silvio Urcuqui-Inchima 1 Maria Eugenia Castano1 Danièle Hernandez- Verdun2 Georges St-Laurent III3 and Ajit Kumar3 Address 1Grupo de Inmunovirología Corporación Biogénesis Universidad de Antioquia . 1226 Medellín Colombia 2Institut Jacques Monod CNRS University Paris VI and Paris VII 2 place Jussieu 75251 Paris Cedex 05 France and 3Department of Biochemistry and Molecular Biology The George Washington University Washington . 20037 USA Email Silvio Urcuqui-Inchima - silviourcuqui@ Maria Eugenia Castano - mcastano@ Danièle Hernandez-Verdun - dhernand@ Georges St-Laurent - gsl@ Ajit Kumar - akumar@ Corresponding author Published 24 November 2006 Received 01 September 2006 Accepted 24 November 2006 Retrovirology 2006 3 83 doi l742-4690-3-83 This article is available from http content 3 1 83 2006 Urcuqui-Inchima 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 The HIV Rev protein is known to facilitate export of incompletely spliced and unspliced viral transcripts to the cytoplasm a necessary step in virus life cycle. The Rev-mediated nucleo-cytoplasmic transport of nascent viral transcripts dependents on interaction of Rev with the RRE RNA structural element present in the target RNAs. The C-terminal variant of dsRNA-binding nuclear protein 90 NF90ctv has been shown to markedly attenuate viral replication in stably transduced HIV-1 target cell line. Here we examined a mechanism of interference of viral .

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