Nuclear relocation of the nephrin and CD2AP-binding protein dendrin promotes apoptosis of podocytes

Nephrin Slit diaphragm Nuclear export signal
DOI: 10.1073/pnas.0700917104 Publication Date: 2007-05-31T00:49:12Z
ABSTRACT
Kidney podocytes and their slit diaphragms (SDs) form the final barrier to urinary protein loss. There is mounting evidence that SD proteins also participate in intracellular signaling pathways. The nephrin serves as a component of complex directly links podocyte junctional integrity actin cytoskeletal dynamics. Another protein, CD2-associated (CD2AP), an adaptor molecule involved homeostasis can repress proapoptotic TGF-beta podocytes. Here we show dendrin, originally identified telencephalic dendrites, constituent complex, where it binds CD2AP. In experimental glomerulonephritis, dendrin relocates from nucleus injured High-dose, TGF-beta1 promotes nuclear import enhances both staurosporine- TGF-beta1-mediated apoptosis. summary, our results identify with properties accumulates response glomerular injury provides molecular target tackle proteinuric kidney diseases. Nuclear relocation may provide mechanism whereby changes could translate into alterations survival under pathological conditions.
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