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Human Molecular Genetics Advance Access published online on May 26, 2004
Human Molecular Genetics, doi:10.1093/hmg/ddh163
© 2004 by Oxford University Press
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Article

The subcellular localization of the ChoRE binding protein, encoded by the Williams-Beuren Syndrome Critical Region gene 14, is regulated by 14-3-3

Giuseppe Merla 1, Cédric Howald 2, Stylianos E. Antonarakis 2, Alexandre Reymond 3*

1 Department of Genetic Medicine and Development, University of Geneva Medical School, Geneva, Switzerland; Servizio Genetica Medica, IRCCS "Casa Sollievo della Sofferenza", San Giovanni Rotondo, Italy
2 Department of Genetic Medicine and Development, University of Geneva Medical School, Geneva, Switzerland
3 Department of Genetic Medicine and Development, University of Geneva Medical School, CMU, 1, rue Michel Servet, 1211 Geneva 4, Switzerland; Center for Integrative Genomics, University of Lausanne, Lausanne, Switzerland

* To whom correspondence should be addressed. E-mail: alexandre.reymond{at}medecine.unige.ch.


  Abstract

The Williams-Beuren syndrome (WBS) is a contiguous gene syndrome caused by chromosomal rearrangements at chromosome band 7q11.23. Several endocrine phenotypes have been described for this clinically complex disorder, in particular impaired glucose tolerance (IGT) and silent diabetes. The WBSCR14 gene, one of the genes mapping to the WBS critical region, encodes a member of the bHLHZip (basic-Helix-Loop-Helix Leucine Zipper) family of transcription factors, which dimerizes with the Max-like protein, Mlx. This heterodimeric complex binds and activates, in a glucose-dependent manner, ChoRE motifs (Carbohydrate Response Element) in the promoter of lipogenic enzymes. We identified five novel WBSCR14-interacting proteins, four 14-3-3 isotypes and NIF3L1, which form a single polypeptide complex in mammalian cells. Phosphatase treatment abrogates the association between WBSCR14 and 14-3-3, as previously shown for multiple 14-3-3 interactors. WBSCR14 is actively exported from the nucleus through a CRM1-dependent mechanism. This translocation is contingent upon the ability to bind 14-3-3. Through this mechanism the 14-3-3 isotypes affect directly the WBSCR14:Mlx complexes transcription activation of lipogenic genes.


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