Nephrin, the key molecule of the glomerular slit diaphragm, is expressed on the surface of
podocytes and is critical in preventing albuminuria. In diabetes, hyperglycemia leads to the
loss of surface expression of nephrin and causes albuminuria. Here, we report a mechanism
that can explain this phenomenon: hyperglycemia directly enhances the rate of nephrin
endocytosis via regulation of the β-arrestin2-nephrin interaction by PKCα. We identified
PKCα and protein interacting with c kinase-1 (PICK1) as nephrin-binding proteins …