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: "Rapamycin-induced inhibition of HTLV-I LTR activity is rescued by c-Myb. | Retrovirology BioMed Central Open Access Rapamycin-induced inhibition of HTLV-I LTR activity is rescued by c-Myb Nicola J Rose 1 and Andrew ML Lever2 Address division of Retrovirology National Institute for Biological Standards and Control Blanche Lane South Mimms Potters Bar Hertfordshire EN6 3QG UK and 2University of Cambridge Department of Medicine Level 5 Addenbrooke s Hospital Hills Road Cambridge. CB2 2QQ UK Email Nicola J Rose - nrose@ Andrew ML Lever - amll1@ Corresponding author Published 3 April 2007 Received 9 January 2007 Retrovirology 2007 4 24 doi 1742-4690-4-24 Accepted 3 April 2007 This article is available from http content 4 1 24 2007 Rose and Lever 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 Rapamycin is an immunosuppressive which represses translation of transcripts harbouring a polypyrimidine motif downstream of the mRNA cap site through the mammalian target of rapamycin complex. It inhibits the abnormal autologous proliferation of T-cell clones containing a transcriptionally active human T-lymphotropic virus type I HTLV-I provirus generated from infected subjects. We showed previously that this effect is independent of the polypyrimidine motifs in the viral long terminal repeat LTR R region suggesting that HTLV-I transcription and not translation is being affected. Here we studied whether rapamycin is having an effect on a specific transcription factor pathway. Further we investigated whether mRNAs encoding transcription factors involved in HTLV-I transcriptional activation specifically CREB Ets and c-Myb are implicated in the rapamycin-sensitivity of the HTLV-I LTR. Results An in vitro analysis of the role of SRE- and .
