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A more recent version of this article appeared on April 21, 2006
Papers In Press, published online ahead of print February 16, 2006
J. Biol. Chem, 10.1074/jbc.M510306200
Submitted on September 20, 2005
Accepted on February 16, 2006
Expression of CD83 is regulated by HuR via a novel cis-active coding region RNA element
Alexander T. Prechtel, Jan Chemnitz, Susann Schirmer, Christina Ehlers, Ines Langbein-Detsch, Jörg Stülke, Marie-Christine Dabauvalle, Ralph H. Kehlenbach, and Joachim Hauber
Cell Biology and Virology, Heinrich-Pette-Institute for Experimental Virology and Immunology, Hamburg D-20251
Corresponding Author: joachim.hauber{at}hpi.uni-hamburg.de
Dendritic cells (DC), the most potent of the antigen-presenting cells are characterized by surface expression of CD83. Here we show that the coding region of CD83 mRNA contains a novel, cis-acting, structured RNA element that binds to HuR, a member of the ELAV family of AU-rich element (ARE) RNA binding proteins. Transient transfection of mammalian cells demonstrates that this CD83 mRNA-derived element acts as a posttranscriptional response element (PRE) in cells that overexpress HuR. Importantly, binding of HuR to the CD83 PRE does not affect mRNA stability. By using RNA interference (RNAi) it is shown that HuR mediates efficient expression of CD83. In particular, HuR is required for cytoplasmic accumulation of CD83 transcripts. Likewise, inhibition of the CRM1 nuclear export pathway by leptomycin B or overexpression of a defective form of the nucleoporin Nup214/CAN diminishes cytoplasmic CD83 mRNA levels. In summary, the presented data demonstrate that the HuR-CRM1 axis affects the nucleocytoplasmic translocation of CD83 mRNA under regular physiological conditions.

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Copyright © 2006 by the American Society for Biochemistry and Molecular Biology.
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