TAILIEUCHUNG - Báo cáo y học: "How HTLV-1 may subvert miRNAs for persistence and transformation"

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: How HTLV-1 may subvert miRNAs for persistence and transformation. | Retrovirology BioMed Central Commentary How HTLV-1 may subvert miRNAs for persistence and transformation Amel B Bouzar1 2 and Luc Willems 1 2 Open Access Address 1Molecular and Cellular Biology lab of the Gembloux Agricultural University FUSAG n 13 avenue Maréchal Juin 5030 Gembloux Belgium and 2Molecular and Cellular Epigenetics Interdisciplinary Cluster for Applied Genoproteomics GIGA of University of Liège ULg avenue de l Hopital n B34 Sart-Tilman 4000 Liège Belgium Email Amel B Bouzar - Luc Willems - Corresponding author Published 12 November 2008 Received 3 November 2008 Accepted 12 November 2008 Retrovirology 2008 5 101 doi l742-4690-5-101 This article is available from http content 5 1 101 2008 Bouzar and Willems 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 Distinct mechanisms are used by viruses to interact with cellular miRNAs. The role of microRNAs in viral replication and persistence ranges from viral-encoded microRNAs to suppressors of RNA interference. Viruses can also exploit cellular miRNAs for influencing cellular metabolism to ensure efficient replication or latency. In particular two recent studies provide examples of how HTLV-1 may co-opt or subvert cellular miRNAs for persistent replication and oncogenic purposes. The pathways modulated by these described miRNAs are critically involved in apoptosis proliferation and innate immune response. Biogenesis of miRNAs MicroRNAs are initially transcribed by RNA polymerase II as a primary miRNA pri-miRNA transcript and processed in the nucleus by RNase III enzyme Drosha and its cofactor DGCR8 1-4 . Cleavage of the pri-miRNA by the Drosha-DGCR8 heterodimer generates a 60-70 .

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