Trans-activation of the human SOX3 promoter by MAZ in NT2/D1 cells

In this study, we examine the role of three highly conserved putative binding sites for Myc-associated zinc finger protein (MAZ) in regulation of the human SOX3 gene expression. Electrophoretic mobility shift and supershift assays indicate that complexes formed at two out of three MAZ sites of the h...

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Bibliographic Details
Published in:Archives of biological sciences 2008, Vol.60 (3), p.379-387
Main Authors: Kovacevic-Grujicic, Natasa, Yokoyama, Kazunari, Stevanovic, Milena
Format: Article
Language:English
Subjects:
MAZ protein
neuronal differentiation
NT2/D1 cells
promoter
SOX3 gene
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Summary:In this study, we examine the role of three highly conserved putative binding sites for Myc-associated zinc finger protein (MAZ) in regulation of the human SOX3 gene expression. Electrophoretic mobility shift and supershift assays indicate that complexes formed at two out of three MAZ sites of the human SOX3 promoter involve ubiquitously expressed MAZ protein. Furthermore, in cotransfection experiments we demonstrate that MAZ acts as a positive regulator of SOX3 gene transcription in both undifferentiated and RA-differentiated NT2/D1 cells. Although MAZ increased both basal and RA-induced promoter activity, our results suggest that MAZ does not contribute to RA inducibility of the SOX3 promoter during neuronal differentiation of NT2/D1 cells. U ovom radu proucavana je uloga tri visoko konzervisana potencijalna mesta vezivanja za "Myc-associated zinc finger protein" (MAZ) u regulaciji ekspresije humanog SOX3 gena. Eseji izmenjene elektroforetske pokretljivosti u prisustvu antitela na MAZ ukazuju da kompleksi koji se formiraju na dva od tri proucavana mesta u okviru SOX3 promotora sadrze MAZ protein. Takodje, u eksperimentima kotransfekcije smo pokazali da MAZ ima ulogu pozitivnog regulatora transkripcije SOX3 gena, kako u nediferenciranim, tako i u diferenciranim NT2/D1 celijama. Iako je MAZ povecao i bazalnu i retinoicnom kiselinom indukovanu promotorsku aktivnost, nasi rezultati ukazuju da ovaj transkripcioni faktor ne doprinosi inducibilnosti SOX3 promotora tokom neuralne diferencijacije u prisustvu retinoicne kiseline.
ISSN:0354-4664
1821-4339
DOI:10.2298/ABS0803379K