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A more recent version of this article appeared on October 11, 2002
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Papers In Press, published online ahead of print August 14, 2002
J. Biol. Chem, 10.1074/jbc.M112273200
Submitted on December 21, 2001
Revised on July 22, 2002
Accepted on August 14, 2002

HLA-G transactivation by CREB: An alternative transactivation pathway to the conserved MHC class I regulatory routes

Sam J. P. Gobin, Paula Biesta, Jurriaan E. M. de Steenwinkel, Gert Datema, and Peter J. Van den Elsen

Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden 2333 ZA

Corresponding Author: gobin{at}LUMC.nl

The expression of HLA-G in extravillous cytotrophoblast cells coincides with a general lack of classical MHC class I expression in this tissue. This differential expression of HLA-G and classical HLA class I molecules in trophoblasts suggests a tight transcriptional control of MHC class I genes. Transactivation of the classical MHC class I genes is mediated by two groups of juxtaposed cis-acting elements which can be viewed as regulatory modules. Both modules are divergent in HLA-G rendering this gene unresponsive to NF-kB, IRF1, and CIITA mediated induction pathways. In this study we searched for alternative regulatory elements in the 1438-bp HLA-G promoter region. HLA-G was not responsive to IFNa, IFNb or IFNg, despite the presence of an upstream ISRE binding IRF1 in vitro. However, the HLA-G promoter contains three CRE/TRE elements with binding affinity for CREB/ATF and Fos/Jun proteins both in vitro and in vivo. In transient transfection assays, it was shown that HLA-G transactivation is regulated by CREB, CBP and p300. Moreover, immunohistochemical analysis demonstrated that HLA-G, and CREB and CBP were co-expressed in extravillous cytotrophoblasts, revealing the in vivo relevance of this transactivation pathway. This implies a unique regulation of HLA-G transcription amongst the MHC class I genes.


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