Expression of CD83 is regulated by HuR via a novel cis-active coding region RNA element.
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Expression of CD83 is regulated by HuR via a novel cis-active coding region RNA element. / Prechtel, Alexander T; Chemnitz, Jan; Schirmer, Susann; Ehlers, Christina; Langbein-Detsch, Ines; Stülke, Jörg; Dabauvalle, Marie-Christine; Kehlenbach, Ralph H; Hauber, Joachim.
In: J BIOL CHEM, Vol. 281, No. 16, 16, 2006, p. 10912-10925.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Expression of CD83 is regulated by HuR via a novel cis-active coding region RNA element.
AU - Prechtel, Alexander T
AU - Chemnitz, Jan
AU - Schirmer, Susann
AU - Ehlers, Christina
AU - Langbein-Detsch, Ines
AU - Stülke, Jörg
AU - Dabauvalle, Marie-Christine
AU - Kehlenbach, Ralph H
AU - Hauber, Joachim
PY - 2006
Y1 - 2006
N2 - Dendritic cells are the most potent of the antigen-presenting cells and 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 RNA-binding proteins. Transient transfection of mammalian cells demonstrated that this CD83 mRNA-derived element acts as a post-transcriptional regulatory element in cells overexpressing HuR. Notably, binding of HuR to the CD83 post-transcriptional regulatory element did not affect mRNA stability. Using RNA interference, we show that HuR mediated efficient expression of CD83. In particular, HuR was 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 diminished cytoplasmic CD83 mRNA levels. In summary, the data presented demonstrate that the HuR-CRM1 axis affects the nucleocytoplasmic translocation of CD83 mRNA under regular physiological conditions.
AB - Dendritic cells are the most potent of the antigen-presenting cells and 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 RNA-binding proteins. Transient transfection of mammalian cells demonstrated that this CD83 mRNA-derived element acts as a post-transcriptional regulatory element in cells overexpressing HuR. Notably, binding of HuR to the CD83 post-transcriptional regulatory element did not affect mRNA stability. Using RNA interference, we show that HuR mediated efficient expression of CD83. In particular, HuR was 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 diminished cytoplasmic CD83 mRNA levels. In summary, the data presented demonstrate that the HuR-CRM1 axis affects the nucleocytoplasmic translocation of CD83 mRNA under regular physiological conditions.
M3 - SCORING: Zeitschriftenaufsatz
VL - 281
SP - 10912
EP - 10925
JO - J BIOL CHEM
JF - J BIOL CHEM
SN - 0021-9258
IS - 16
M1 - 16
ER -