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: Matrin 3 is a co-factor for HIV-1 Rev in regulating post-transcriptional viral gene expression. | Yedavalli and Jeang Retrovirology 2011 8 61 http content 8 1 61 RETR0VIR0L0GY RESEARCH Open Access Matrin 3 is a co-factor for HIV-1 Rev in regulating post-transcriptional viral gene expression Venkat SRK Yedavalli and Kuan-Teh Jeang Abstract Post-transcriptional regulation of HIV-1 gene expression is mediated by interactions between viral transcripts and viral cellular proteins. For HIV-1 post-transcriptional nuclear control allows for the export of intron-containing RNAs which are normally retained in the nucleus. Specific signals on the viral RNAs such as instability sequences INS and Rev responsive element RRE are binding sites for viral and cellular factors that serve to regulate RNA-export. The HIV-1 encoded viral Rev protein binds to the RRE found on unspliced and incompletely spliced viral RNAs. Binding by Rev directs the export of these RNAs from the nucleus to the cytoplasm. Previously Rev co-factors have been found to include cellular factors such as CRM1 DDX3 PIMT and others. In this work the nuclear matrix protein Matrin 3 is shown to bind Rev RRE-containing viral RNA. This binding interaction stabilizes unspliced and partially spliced HIV-1 transcripts leading to increased cytoplasmic expression of these viral RNAs. Keywords Matrin 3 HIV-1 Rev RNA export nuclear matrix protein Background The nucleus is a highly organized structure. Chromosomes occupy discrete regions and specific proteins and nucleic acids are enriched in subnuclear structures such as nuclear lamina nucleoli Cajal bodies nuclear speckles and paraspeckles 1-6 . The nuclear matrix a network of underlying filaments in the cell nucleus shapes the nuclear architecture and functions in genome maintenance transcription and RNA metabolism 7-17 . Accordingly the nuclear matrix has important roles in tissue development and cellular proliferation and the disruption of nuclear organization is often correlated with disease states such as the loss of subnuclear pro-myelocytic
