Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Retrovirology cung cấp cho các bạn kiến thức về ngành y đề tài: Identification of a novel motif responsible for the distinctive transforming activity of human T-cell leukemia virus (HTLV) type 1 Tax1 protein from HTLV-2 Tax2. | Retrovirology BioMed Central Research Identification of a novel motif responsible for the distinctive transforming activity of human T-cell leukemia virus HTLV type 1 Taxi protein from HTLV-2 Tax2 Toshiyuki Shoji11 2 Masaya Higuchi11 Rie Kondo1 Masahiko Takahashi1 Masayasu Oie1 Yuetsu Tanaka3 Yutaka Aoyagi2 and Masahiro Fujii 1 Open Access Address 1Division of Virology Niigata University Graduate School of Medical and Dental Sciences 1-757 Asahimachi-Dori Niigata 951-8510 Japan 2Division of Gastroenterology and Hepatology Niigata University Graduate School of Medical and Dental Sciences 1-757 Asahimachi-Dori Niigata 951-8510 Japan and 3Department of Immunology Graduate School and Faculty of Medicine University of the Ryukyus Uehara 207 Nishihara-cho Nakagami-gun Okinawa 903-0215 Japan Email Toshiyuki Shoji - shoji-t@ Masaya Higuchi - mhiguchi@ Rie Kondo - rierie-j@ Masahiko Takahashi - masahiko@ Masayasu Oie - moie@ Yuetsu Tanaka - yuetsu@ Yutaka Aoyagi - aoy@ Masahiro Fujii - fujiimas@ Corresponding author tEqual contributors Published 17 September 2009 Received 12 May 2009 Accepted 17 September 2009 Retrovirology 2009 6 83 doi l742-4690-6-83 This article is available from http content 6 1 83 2009 Shoji 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 1 HTLV-1 is a causative agent of adult T-cell leukemia ATL whereas its relative HTLV-2 is not associated with any malignancies including ATL. HTLV-1 Tax1 transformed a T-cell line from interleukin IL -2-dependent growth to IL-2-independent growth with
