Medical Journals

An Evolutionarily Conserved Mechanism for Microrna-223 Expression Revealed by Microrna Gene Profiling.

Authors:
  • Fukao Taro
  • Fukuda Yoko
  • Kiga Kotaro
  • Sharif Jafar
  • Hino Kimihiro
  • Enomoto Yutaka
  • Kawamura Aya
  • Nakamura Kaito
  • Takeuchi Tsutomu
  • Tanabe Masanobu

From: Department of Chemistry and Biotechnology, Graduate School of Engineering, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8656, Japan. tarofukao@2002.jukuin.keio.ac.jp

Cell

  • Publish Date: May 2007
  • ISSN: 0092-8674
  • Volume: 129
  • Issue: 3
  • Pages: 617-31
  • Medium: Print
  • Language: English
  • Citation (JAMA): Fukao Taro, Fukuda Yoko, Kiga Kotaro, et al. An Evolutionarily Conserved Mechanism for Microrna-223 Expression Revealed by Microrna Gene Profiling.. Cell May 2007;129:617-31

Abstract

Many microRNAs (miRNAs) are evolutionarily conserved and have intriguing expression patterns. Tissue and/or time-specific expressions of some miRNAs are presumably controlled by unique cis-acting regulatory elements that coevolved with the miRNA sequences. Exploiting bioinformatics, we identified several miRNAs whose primary transcripts could be regulated by conserved genomic elements proximal to their transcription start sites. Such miRNAs include microRNA-223 (miR-223), which is reportedly controlled by a unique regulatory mechanism during granulopoiesis. Here, we define a mechanism distinct from that previously proposed to regulate miR-223 expression. We find that the mir-223 gene resembles a “myeloid gene” and might be driven by the myeloid transcription factors, PU.1 and C/EBPs. This mechanism is specified by the conserved proximal cis-regulatory element and might be common among different species. Hence, it needs to be considered that two distinct mechanisms that would play critical roles in myeloid functions and differentiation are actually concerned with the regulation of miR-223.

Mesh Headings (Keywords): Animals, CCAAT-Enhancer-Binding Proteins, Cell Line, Tumor, Conserved Sequence, Evolution, Molecular, Gene Expression Profiling, Gene Expression Regulation, Genome, Humans, Mice, MicroRNAs, Promoter Regions (Genetics), Proto-Oncogene Proteins, Trans-Activators, Transcription Factors, Transcription, Genetic


Check for Full Text / PubMed Unique Identifier (PMID): 17482553


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

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The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.


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