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Papers In Press, published online ahead of print September 18, 2001
J. Biol. Chem, 10.1074/jbc.C100452200
Submitted on August 13, 2001
Revised on September 18, 2001
Accepted on September 18, 2001

Interaction with podocin facilitates nephrin signaling

Tobias B. Huber, Michael Köttgen, Birgit Schilling, Gerd Walz, and Thomas Benzing

Department of Medicine, Nephrology, University Hospital of Freiburg, Freiburg 79106

Corresponding Author: walz{at}med1.ukl.uni-freiburg.de

Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria. In addition, mice lacking CD2-associated protein (CD2AP) develop a nephrotic syndrome that resembles NPHS mutations, suggesting that all three proteins are essential for the integrity of glomerular podocytes. Although the precise glomerular function of either protein remains unknown, it has been suggested that nephrin forms zipper-like interactions to maintain the structure of podocyte foot processes. We demonstrate now that nephrin is a signaling molecule, which stimulates mitogen-activated protein kinases. Nephrin-induced signaling is greatly enhanced by podocin, which binds to the cytoplasmic tail of nephrin. Mutational analysis suggests that abnormal or inefficient signaling through the nephrin-podocin complex contribute to the development of podocyte dysfunction and proteinuria.


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