tailieunhanh - Báo cáo y học: "DNA double strand break repair enzymes function at multiple steps in retroviral infection"

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: DNA double strand break repair enzymes function at multiple steps in retroviral infection. | Retrovirology BioMed Central Open Access DNA double strand break repair enzymes function at multiple steps in retroviral infection Yasuteru Sakurai1 2 Kenshi Komatsu3 Kazunaga Agematsu4 and Masao Matsuoka 1 Address laboratory ofVirus Control Institute for Virus Research Kyoto University 53 Shogoin Kawahara-cho Sakyo-ku Kyoto 606-8507 Japan laboratory of Cell Regulation and Molecular Network Graduate School of Biostudies Kyoto University Kyoto 606-8501 Japan 3Department of Genome Repair Dynamics Radiation Biology Center Kyoto University Yoshidakonoe-cho Sakyo-ku Kyoto 606-8501 Japan and 4Department of Infection and Host Defense Graduate School of Medicine Shinshu University 3-1-1 Asahi Matsumoto Nagano 390-8621 Japan Email Yasuteru Sakurai - ysakurai@ Kenshi Komatsu - komatsu@ Kazunaga Agematsu - agemts_k@ Masao Matsuoka - mmatsuok@ Corresponding author Published 15 December 2009 Received 9 September 2009 Accepted 15 December 2009 Retrovirology 2009 6 114 doi l742-4690-6-114 This article is available from http content 6 1 1 14 2009 Sakurai 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 DNA double strand break DSB repair enzymes are thought to be necessary for retroviral infection especially for the post-integration repair and circularization of viral cDNA. However the detailed roles of DSB repair enzymes in retroviral infection remain to be elucidated. Results A GFP reporter assay showed that the infectivity of an HIV-based vector decreased in ATM- and DNA-PKcs-deficient cells when compared with their complemented cells while that of an MLV-based vector was diminished in Mre11- and .

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