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Am J Physiol Renal Physiol (May 7, 2002). doi:10.1152/ajprenal.00128.2002
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Articles in PresS, published online ahead of print May 7, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00128.2002
Submitted on April 3, 2002
Accepted on May 6, 2002

Regulation of the Kidney-Specific Ksp-Cadherin Gene Promoter by Hepatocyte Nuclear Factor-1ß (HNF-1ß)

Yun Bai1, Marco Pontoglio2, Thomas Hiesberger1, Angus M Sinclair1, and Peter` Igarashi1*

1 Division of Nephrology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA
2 Developmental Biology, Centre National de la Recherche Scientifique, Institut Pasteur, Paris, France

* To whom correspondence should be addressed. E-mail: peter.igarashi{at}utsouthwestern.edu.

Ksp-cadherin is a tissue-specific member of the cadherin family that is expressed exclusively in the kidney and developing genitourinary tract. Recent studies have shown that the proximal 250 bp of the Ksp-cadherin gene promoter is sufficient to direct tissue-specific gene expression in vivo and in vitro. The proximal 120 bp of the promoter is evolutionarily conserved between mouse and human and contains a DNase I hypersensitive site that is kidney cell-specific. At position -55, the promoter contains a consensus recognition site for hepatocyte nuclear factor-1 (HNF-1). Mutations of the consensus HNF-1 site and downstream GC-boxes inhibit promoter activity in transfected cells. HNF-1{alpha} and HNF-1ß bind specifically to the -55 site, and both proteins transactivate the promoter directly. Expression of Ksp-cadherin is not altered in the kidneys of HNF1{alpha}-deficient mice. However, expression of a gain-of-function HNF-1ß mutant stimulates Ksp-cadherin promoter activity in transfected cells, whereas expression of a dominant-negative mutant inhibits activity. These studies identify Ksp-cadherin as the first kidney-specific promoter that has been shown to be regulated by HNF-1ß. Mutations of HNF-1ß, as occur in humans with inherited renal cysts and diabetes, may cause dysregulated Ksp-cadherin promoter activity.




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