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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Minireview cung cấp cho các bạn kiến thức về ngành y đề tài: Preferential regulation of duplicated genes by microRNAs in mammals. | Open Access Research Preferential regulation of duplicated genes by microRNAs in mammals Jingjing Li Gabriel Musso n and Zhaolei Zhang Addresses Department of Molecular Genetics University of Toronto 1 King s College Circle Toronto ON M5S 1A8 Canada. tDonnelly Centre for Cellular and Biomolecular Research University of Toronto 160 College Street Toronto ON M5S 3E1 Canada. Banting and Best Department of Medical Research University of Toronto 160 College Street Toronto ON M5S 3E1 Canada. Correspondence Zhaolei Zhang. Email Zhaolei.Zhang@utoronto.ca Published 26 August 2008 Genome Biology 2008 9 RI32 doi I0.II86 gb-2008-9-8-rI 32 The electronic version of this article is the complete one and can be found online at http genomebiology.com 2008 9 8 RI32 Received 7 March 2008 Revised 5 July 2008 Accepted 26 August 2008 2008 Li et al. 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 Although recent advances have been made in identifying and analyzing instances of microRNA-mediated gene regulation it remains unclear by what mechanisms attenuation of transcript expression through microRNAs becomes an integral part of post-transcriptional modification and it is even less clear to what extent this process occurs for mammalian gene duplicates paralogs . Specifically while mammalian paralogs are known to overcome their initial complete functional redundancy through variation in regulation and expression the potential involvement of microRNAs in this process has not been investigated. Results We comprehensively investigated the impact of microRNA-mediated post-transcriptional regulation on duplicated genes in human and mouse. Using predicted targets derived from several analysis methods we report the following .
