We demonstrate that both nephrin and CD2AP interact with the p 85 regulatory subunit of phosphoinositide 3 OH kinase ( PI3K ) in vivo , recruit PI3K to the plasma membrane , and , together with podocin , stimulate PI3K dependent AKT signaling in podocytes . ^^^ Our findings reveal a novel role for the slit diaphragm proteins nephrin , CD2AP , and podocin and demonstrate that these three proteins , in addition to their structural functions , initiate PI3K / AKT dependent signal transduction in glomerular podocytes . . ^^^ |