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Báo cáo hóa học: " HDAC inhibitors stimulate viral transcription by multiple mechanisms"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: HDAC inhibitors stimulate viral transcription by multiple mechanisms | Virology Journal BioMed Central Research HDAC inhibitors stimulate viral transcription by multiple mechanisms Lata Balakrishnan and Barry Milavetz Open Access Address Department of Biochemistry and Molecular Biology University of North Dakota Grand Forks North Dakota USA Email Lata Balakrishnan - lbalakrishnan@medicine.nodak.edu Barry Milavetz - bmilavetz@medicine.nodak.edu Corresponding author Published 19 March 2008 Received 25 January 2008 Accepted 19 March 2008 Virology journal 2008 5 43 doi l0.ll86 l743-422X-5-43 This article is available from http www.virologyj.cOm content 5 1 43 2008 Balakrishnan and Milavetz licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background The effects of histone deacetylase inhibitor HDACi treatment on SV40 transcription and replication were determined by monitoring the levels of early and late expression the extent of replication and the percentage of SV40 minichromosomes capable of transcription and replication following treatment with sodium butyrate NaBu and trichostatin A TSA . Results The HDACi treatment was found to maximally stimulate early transcription at early times and late transcription at late times through increased numbers of minichromosomes which carry RNA polymerase II RNAPII transcription complexes and increased occupancy of the transcribing minichromosomes by RNAPII. HDACi treatment also partially relieved the normal downregulation of early transcription by T-antigen seen later in infection. The increased recruitment of transcribing minichromosomes at late times was correlated to a corresponding reduction in SV40 replication and the percentage of minichromosomes capable of replication. Conclusion These results suggest that histone deacetylation plays a critical