Abstract
Proteinuria in several glomerular diseases results from dysfunction of the slit diaphragm, a cell-cell junction of glomerular epithelial cells (podocytes). Ephrin-B1 and its related molecule NHERF 2 are novel essential components of the slit diaphragm. Ephrin-B1 interacts with nephrin via the extra-cellular domain and interacts with NHERF2 via the cytoplasmic site. In the proteinuric state induced by the stimulation to nephrin, nephrin and ephrin-B1 are phosphorylated, and NHERF2 is de- phosphorylated and consequent disruption of the linkage and downregulation of nephrin, ephrin-B1 and NHERF2 are a critical pathogenic event of podocyte injury. Keywords: Podocyte; Slit Diaphragm; Ephrin-B1; Nephrin; NHERF2
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