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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

WT1 activates a glomerular-specific enhancer identified from the human nephrin gene.

The glomerular filtration barrier separates the blood from the urinary space. Nephrin is a transmembrane protein that belongs to the immunoglobulin superfamily and is localized to the slit diaphragms that are a critical component of this filtration barrier. Mutations in the nephrin gene (NPHS1) lead to congenital Finnish nephropathy, whereas alterations in the level of nephrin expression have been identified in a wide range of acquired glomerular diseases. A 186-bp fragment from the human NPHS1 promoter is capable of directing podocyte-specific expression of a beta-galactosidase transgene when placed in front of a heterologous minimal promoter in transgenic mice. The Wilms tumor suppressor gene (WT1) is a zinc-finger-containing transcription factor that is coexpressed with NPHS1 in differentiated podocytes; gel shift binding assays demonstrate that a recombinant WT1 protein can bind and activate the 186-bp NPHS1 fragment in a sequence-specific manner. Taken together, these results suggest that WT1 may be required for regulation of the NPHS1 gene in vivo.[1]


  1. WT1 activates a glomerular-specific enhancer identified from the human nephrin gene. Guo, G., Morrison, D.J., Licht, J.D., Quaggin, S.E. J. Am. Soc. Nephrol. (2004) [Pubmed]
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