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:"Dephosphorylation of CDK9 by protein phosphatase 2A and protein phosphatase-1 in Tat-activated HIV-1 transcription | Retrovirology BioMed Central Research Open Access Dephosphorylation of CDK9 by protein phosphatase 2A and protein phosphatase-l in Tat-activated HIV-I transcription Tatyana Ammosova 1 Kareem Washington1 Zufan Debebe1 John Brady3 and Sergei Nekhai 1 2 Address 1Center for Sickle Cell Disease Howard University 2121 Georgia Ave. . Washington DC 20059 USA 2Department of Biochemistry and Molecular Biology Howard University College of Medicine 520 W Street . Washington DC 20059 USA and 3Virus Tumor Biology Section LRBGE National Cancer Institute Bethesda MD 20892 USA Email Tatyana Ammosova - tammosova@ Kareem Washington - ER223LK@ Zufan Debebe - zdebebe@ John Brady - bradyj@ Sergei Nekhai - snekhai@ Corresponding author Published 27 July 2005 Received 15 March 2005 Retrovirology 2005 2 47 doi 1742-4690-2-47 Accepted 27 July 2005 This article is available from http content 2 1 47 2005 Ammosova 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 HIV-1 Tat protein recruits human positive transcription elongation factor P-TEFb consisting of CDK9 and cyclin T1 to HIV-1 transactivation response TAR RNA. CDK9 is maintained in dephosphorylated state by TFIIH and undergo phosphorylation upon the dissociation of TFIIH. Thus dephosphorylation of CDK9 prior to its association with HIV-1 preinitiation complex might be important for HIV-1 transcription. Others and we previously showed that protein phosphatase-2A and protein phosphatase-1 regulates HIV-1 transcription. In the present study we analyze relative contribution of PP2A and PP1 to dephosphorylation of CDK9 and to HIV- 1 transcription in vitro and in vivo. Results In vitro PP2A .
