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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: "Activation of HIV-1 expression and replication by cGMP dependent protein kinase type 1-β (PKG1β). | Retrovirology BioMed Central Short report Open Access Activation of HIV-1 expression and replication by cGMP dependent protein kinase type 1-p PKG1 p Jia Hai Lee Venkat RK Yedavalli and Kuan-Teh Jeang Address Molecular Virology Section Laboratory of Molecular Microbiology National Institute of Allergy and Infectious Diseases National Institutes of Health Bethesda Maryland 20892-0460 USA Email Jia Hai Lee - jiahai@yahoo.com Venkat RK Yedavalli - vyedavalli@mail.nih.gov Kuan-Teh Jeang - kjeang@niaid.nih.gov Corresponding author Published 13 December 2007 Received 25 October 2007 Accepted 13 December 2007 Retrovirology 2007 4 91 doi l0.ll86 l 742-4690-4-91 This article is available from http www.retrovirology.cOm content 4 1 91 2007 Lee et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract The effect of cGMP cyclic GMP dependent protein kinase 1-P PKG1-P and cGMP analogues on transcriptional activity and replication of human immunodeficiency virus type 1 HIV-1 was investigated. Transfection of PKG1 p expression plasmid increased expression from an HIV-1 LTR-reporter as well as from an infectious HIV-l molecular clone pNL4-3. Treatment of HIV-l AD8-infected monocyte derived macrophages MDMs with cGMP agonists and cGMP antagonists caused respectively increased and decreased virus replication. These findings provide evidence that cGMP and PKG serve to regulate HIV-1 infection in human cells. Findings Previously nitric oxide NO was postulated to have a negative effect on HIV-1 replication through a cGMP-inde-pendent route 1 . However it was not characterized as to how this cGMP-independent effect manifested mechanistically. On the other hand it is well-accepted that a major intracellular signaling pathway for NO is .
