Increasing evidence implicates activation of NF-κB in a variety of glomerular diseases, but
the mechanisms involved are unknown. Here, upregulation of NF-κB in the podocytes of
transgenic mice resulted in glomerulosclerosis and proteinuria. Absence of the podocyte
protein nephrin resulted in NF-κB activation, suggesting that nephrin negatively regulates
the NF-κB pathway. Signal transduction assays supported a functional relationship between
nephrin and NF-κB and suggested the involvement of atypical protein kinase C (aPKCζ/λ/ι) …