FIGURE 10.

Schematic presentation of the proposed TAT-Neph1CD action. The tyrosine phosphorylation of endogenous Neph1 is increased in response to PAN that induces downstream signaling leading to cytoskeleton damage and kidney malfunction. Transduction of TAT-Neph1CD competes for endogenous Neph1 interactions, thereby blocking Neph1 phosphorylation and inhibiting the downstream signaling. Thus, the transduced cells are unable to respond to injury and are therefore protected from the PAN-induced podocyte damage.