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Nucleic Acids Research 2004 32(14):4340-4350; doi:10.1093/nar/gkh735
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Published online 17 August 2004

Nucleic Acids Research, Vol. 32 No. 14 © Oxford University Press 2004; all rights reserved

MAGE-A1 interacts with adaptor SKIP and the deacetylase HDAC1 to repress transcription

Sandra Laduron, Rachel Deplus1, Sifang Zhou2, Olga Kholmanskikh, Danièle Godelaine, Charles De Smet, S. Diane Hayward2, François Fuks1, Thierry Boon and Etienne De Plaen*

Ludwig Institute for Cancer Research, Brussels branch, and Cellular Genetics Unit, Université Catholique de Louvain, Brussels B1200, Belgium, 1 Laboratory of Molecular Virology, C.P. 614, Faculty of Medicine, Free University of Brussels, B1070, Belgium and 2 Department of Pharmacology and Molecular Science, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA

* To whom correspondence should be addressed at Ludwig Institute for Cancer Research, 74 Avenue Hippocrate-UCL 74.59, B1200 Brussels, Belgium. Tel: +322 764 7479; Fax: +322 762 9405; Email: Etienne.Deplaen{at}bru.licr.org

Received as resubmission June 27, 2004; Accepted July 12, 2004

MAGE-A1 belongs to a family of 12 genes that are active in various types of tumors and silent in normal tissues except in male germ-line cells. The MAGE-encoded antigens recognized by T cells are highly tumor-specific targets for T cell-oriented cancer immunotherapy. The function of MAGE-A1 is currently unknown. To analyze it, we attempted to identify protein partners of MAGE-A1. Using yeast two-hybrid screening, we detected an interaction between MAGE-A1 and Ski Interacting Protein (SKIP). SKIP is a transcriptional regulator that connects DNA-binding proteins to proteins that either activate or repress transcription. We show that MAGE-A1 inhibits the activity of a SKIP-interacting transactivator, namely the intracellular part of Notch1. Deletion analysis indicated that this inhibition requires the binding of MAGE-A1 to SKIP. Moreover, MAGE-A1 was found to actively repress transcription by binding and recruiting histone deacetylase 1 (HDAC1). Our results indicate that by binding to SKIP and by recruiting HDACs, MAGE-A1 can act as a potent transcriptional repressor. MAGE-A1 could therefore participate in the setting of specific gene expression patterns for tumor cell growth or spermatogenesis.


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