tailieunhanh - Báo cáo y học: " Kaposi's sarcoma associated herpes virus-encoded viral FLICE inhibitory protein activates transcription from HIV-1 Long Terminal Repeat via the classical NF-κB pathway and functionally cooperates with Tat"

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: Kaposi's sarcoma associated herpes virus-encoded viral FLICE inhibitory protein activates transcription from HIV-1 Long Terminal Repeat via the classical NF-κB pathway and functionally cooperates with Tat | Retrovirology BioMed Central Research Open Access Kaposi s sarcoma associated herpes virus-encoded viral FLICE inhibitory protein activates transcription from HIV-1 Long Terminal Repeat via the classical NF-kB pathway and functionally cooperates with Tat Qinmiao Sun1 Hittu Matta1 2 and Preet M Chaudhary 1 2 Address 1Hamon Center for Therapeutic Oncology Research UT Southwestern Medical Center Dallas TX 75390-8593 USA and 2Department of Medicine Division of Hematology-Oncology and the Hillman Cancer Center University of Pittsburgh PA 15213 USA Email Qinmiao Sun - Hittu Matta - mattah@ Preet M Chaudhary - chaudharypm@ Corresponding author Published 15 February 2005 Received 24 September 2004 Retrovirology 2005 2 9 doi 1742-4690-2-9 Accepted I5 February 2005 This article is available from http content 2 1 9 2005 Sun 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 nuclear transcription factor NF-kB binds to the HIV-1 long terminal repeat LTR and is a key regulator of HIV-1 gene expression in cells latently infected with this virus. In this report we have analyzed the ability of Kaposi s sarcoma associate herpes virus KSHV also known as Human Herpes virus 8 -encoded viral FLIP Fas-associated death domain-like IL-1 betaconverting enzyme inhibitory protein K13 to activate the HIV-1 LTR. Results We present evidence that vFLIP K13 activates HIV-1 LTR via the activation of the classical NF-kB pathway involving c-Rel p65 and p50 subunits. K13-induced HIV-1 LTR transcriptional activation requires the cooperative interaction of all three components of the IKK complex and can be effectively blocked by inhibitors of the classical .