tailieunhanh - Báo cáo y học: " Role of Tax protein in human T-cell leukemia virus type-I leukemogenicity"

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: Role of Tax protein in human T-cell leukemia virus type-I leukemogenicity | Retrovirology BioMed Central Review Role of Tax protein in human T-cell leukemia virus type-I leukemogenicity Inbal Azran Yana Schavinsky-Khrapunsky and Mordechai Aboud Open Access Address Department of Microbiology and Immunology and Cancer Research Center Faculty of Health Sciences Ben Gurion University of the Negev Beer Sheva 84105 Israel Email Inbal Azran - azron@ Yana Schavinsky-Khrapunsky - shavinsk@ Mordechai Aboud - aboud@ Corresponding author Published 13 August 2004 Received 26 June 2004 Retrovirology 2004 1 20 doi 1742-4690-1-20 Accepted 13 August 2004 This article is available from http content 1 1 20 2004 Azran 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 HTLV-1 is the etiological agent of adult T-cell leukemia ATL the neurological syndrome TSP HAM and certain other clinical disorders. The viral Tax protein is considered to play a central role in the process leading to ATL. Tax modulates the expression of many viral and cellular genes through the CREB ATF- SRF- and NF-KB-associated pathways. In addition Tax employs the CBP p300 and p CAF co-activators for implementing the full transcriptional activation competence of each of these pathways. Tax also affects the function of various other regulatory proteins by direct protein-protein interaction. Through these activities Tax sets the infected T-cells into continuous uncontrolled replication and destabilizes their genome by interfering with the function of telomerase and topoisomerase-I and by inhibiting DNA repair. Furthermore Tax prevents cell cycle arrest and apoptosis that would otherwise be induced by the unrepaired DNA damage and enables thereby accumulation of