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Biochem Biophys Res Commun. 1999 Jul 14;260(3):600-4.

Transcription factor NF1 mediates repression of the GLUT4 promoter by cyclic-AMP.

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Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, 21287-2520, USA.


Prolonged treatment of 3T3-L1 adipocytes with 8-Br-cAMP decreases expression of GLUT4, the insulin-responsive glucose transporter. Expression of a promoter-reporter gene construct that contained 785 base pairs of 5'-flanking region of the murine GLUT4 gene was down regulated by 8-Br-cAMP (p < 0.001), whereas expression of constructs that contained 641 or 469 base pairs of 5'-flanking region was not. A reporter gene construct in which bases -706 to -676 were deleted was not repressed by 8-Br-cAMP, thereby identifying a 30 bp region as necessary for repression of the GLUT4 promoter by 8-Br-cAMP. Mutations in this regulatory element that disrupt binding of the transcription factor NF1 abolish the 8-Br-cAMP-induced repression of the gene. Although insulin and cAMP both repress the GLUT4 promoter through this cis-element, they appear to do this through different mechanisms, as treatment with 8-Br-cAMP does not induce the phosphorylation of NF1 that is induced by insulin treatment.

[Indexed for MEDLINE]

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