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Am J Physiol Renal Physiol 283: F839-F851, 2002. First published May 7, 2002; doi:10.1152/ajprenal.00128.2002
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Vol. 283, Issue 4, F839-F851, October 2002

Regulation of kidney-specific Ksp-cadherin gene promoter by hepatocyte nuclear factor-1beta

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 at Dallas, Dallas, Texas 75390; and 2 Unité d'Expression Génétique et Maladies, Centre National de la Recherche Scientifique URA 1644, Département de Biologie du Développement, Institut Pasteur, 75724 Paris cedex 15, France

Kidney-specific cadherin (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 are sufficient to direct tissue-specific gene expression in vivo and in vitro. The proximal 120 bp of the promoter are evolutionarily conserved between mouse and human and contain 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-1alpha and HNF-1beta bind specifically to the -55 site, and both proteins transactivate the promoter directly. Expression of Ksp-cadherin is not altered in the kidneys of HNF-1alpha -deficient mice. However, expression of a gain-of-function HNF-1beta 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-1beta . Mutations of HNF-1beta , as occur in humans with inherited renal cysts and diabetes, may cause dysregulated Ksp-cadherin promoter activity.

transcription factor; kidney-specific gene regulation; mouse inner medullary collecting duct-3 cells; deoxyribonuclease hypersensitive sites; maturity-onset diabetes of the young


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