tailieunhanh - Báo cáo y học: " Silencing of human T-cell leukemia virus type I gene transcription by epigenetic mechanisms"

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:Silencing of human T-cell leukemia virus type I gene transcription by epigenetic mechanisms | Retrovirology BioMed Central Research Open Access Silencing of human T-cell leukemia virus type I gene transcription by epigenetic mechanisms Yuko Taniguchi1 Kisato Nosaka1 2 Jun-ichirou Yasunaga1 Michiyuki Maeda3 Nancy Mueller4 Akihiko Okayama5 and Masao Matsuoka 1 Address laboratory of Virus Immunology Institute for Virus Research Kyoto University Kyoto 606-8507 Japan 2Department of Hematology Kumamoto University School of Medicine Kumamoto 860-8556 Japan 3Laboratory of Infection and Prevention Institute for Virus Research Kyoto University Kyoto 606-8507 Japan 4Department of Epidemiology Harvard School of Public Health Boston Massachusetts 02115 USA and 5Department of Laboratory Medicine Faculty of Medicine University of Miyazaki Miyazaki 889-1692 Japan Email Yuko Taniguchi - yutanigu@ Kisato Nosaka - knosaka@ Jun- ichirou Yasunaga - jyasunag@ Michiyuki Maeda - mimaeda@ Nancy Mueller - nmueller@ Akihiko Okayama - okayama@ Masao Matsuoka - mmatsuok@ Corresponding author Published 22 October 2005 Received 31 August 2005 Accepted 22 October 2005 Retrovirology 2005 2 64 doi l 742-4690-2-64 H This article is available from http content 2 1 64 2005 Taniguchi 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 Human T-cell leukemia virus type I HTLV-I causes adult T-cell leukemia ATL after a long latent period. Among accessory genes encoded by HTLV-I the tax gene is thought to play a central role in oncogenesis. However Tax expression is disrupted by several mechanims including genetic changes of the tax gene deletion hypermethylation of 5 .

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