SUN-098 MUTATION OF p66SHC IN RATS CAUSES INCREASED H2O2 PRODUCTION AND LEADS TO REDUCED NUMBER OF GLOMERULI

Shc proteins, products of Shc1 gene, exists in three functionally distinct isoforms (p46Shc, p52Shc, and p66Shc) that serve as intracellular adaptors for several key signaling pathways involved in renal pathologies. Adaptor protein p66Shc contributes to the pathogenesis of oxidative stress-related diseases and is known to regulate the sensitivity to oxidative stress. The objective of this study was to test the hypothesis that abnormal p66Shc-mediated ROS production could be critically involved in the development of nephrons during nephrogenesis.