POS-395 P66SHC-MEDIATED H2O2 PRODUCTION IMPAIRS NEPHROGENESIS CAUSING REDUCTION OF NUMBER OF GLOMERULI

Adaptor protein p66Shc, one of three Shc1 gene products, 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 reactive oxygen species (ROS) production could be critically involved in the development of nephrons during nephrogenesis. p66Shc ability to promote oxidative stress-related diseases requires phosphorylation of serine 36 residue (Ser-36), which causes conformation change and consequent translocation of p66Shc to the mitochondria where it increases the production of ROS.