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MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Control of Glut1 promoter activity under basal conditions and in response to hyperosmolarity: role of Sp1

Department of Physiology and Biophysics and Department of Medicine, Case Western Reserve University, Cleveland, Ohio

Submitted 1 March 2005 ; accepted in final form 6 September 2005

We previously identified (Hwang DY and Ismail-Beigi F. Am J Physiol Cell Physiol 281: C1365–C1372, 2001) a 44-bp GC-rich segment of the rat proximal glucose transporter (Glut)1 promoter, located at –104 to –61, as necessary for basal transcription of the Glut1 gene. Using deletion and mutational analysis and expression of transfected reporter constructs, we report in the present study that mutation of the Sp1 site located within this segment of the promoter leads to a marked (4-fold) decrease in basal promoter activity. Double mutations located in the Sp1 site and in a second downstream GC-rich region (–71 to –51) did not cause a further decrease in promoter activity. Gel shift and supershift assays verified the importance of the Sp1 site. Exposure of cells to trichostatin A resulted in increased expression of the endogenous Glut1 as well as the transfected wild-type construct. Finally, the presence of the Sp1 site was found to be essential for the positive response of the promoter to hyperosmolarity. We conclude that the consensus Sp1 site located in the rat proximal Glut1 promoter is necessary and sufficient for basal expression of the Glut1 gene, as well as for its response to hyperosmolarity.

Glut1 messenger RNA; Sp1; Sp3; electrophoretic mobility shift assay

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