Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: Dominant negative mutant Cyclin T1 proteins inhibit HIV transcription by specifically degrading Tat. | Retrovirology BioMed Central Research Dominant negative mutant Cyclin T1 proteins inhibit HIV transcription by specifically degrading Tat Julie K Jadlowsky1 Masanori Nojima1 Antje Schulte2 Matthias Geyer2 Takashi Okamoto3 and Koh Fujinaga 1 Open Access Address division of Infectious Diseases Department of Medicine Department of Molecular Biology and Microbiology Case Western Reserve University School of Medicine Cleveland Ohio USA 2Max-Planck-Institut fur molekulare Physiologie Abteilung Physikalische Biochemie Dortmund Germany and 3Department of Molecular and Cellular Biology Nagoya City University Graduate School of Medical Sciences Nagoya Japan Email Julie K Jadlowsky - Masanori Nojima - nojima@ Antje Schulte - Matthias Geyer - Takashi Okamoto - tokamoto@ Koh Fujinaga - kxf32@ Corresponding author Published II July 2008 Received 9 April 2008 Retrovirology 2008 5 63 doi 1742-4690-5-63 Accepted 11 July 2008 This article is available from http content 5 1 63 2008 Jadlowsky 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 positive transcription elongation factor b P-TEFb is an essential cellular cofactor for the transcription of the human immunodeficiency virus type 1 HIV-1 . The cyclin T1 CycT1 subunit of P-TEFb associates with a viral protein Tat at the transactivation response element TAR . This represents a critical and necessary step for the stimulation of transcriptional elongation. Therefore CycT1 may serve as a potential target for the development of anti-HIV therapies. Results To create effective inhibitors of HIV transcription
