Supplementary Material for: Direct Interaction of α-Synuclein and AKT Regulates IGF-1 Signaling: Implication of Parkinson Disease [article]

J.-Y. Chung, S.-J. Lee, S.-H. Lee, Y.S. Jung, N.-C. Ha, W. Seol, B.-J. Park
2017 Figshare  
Genetic mutation of α-synuclein (α-SYN) is clearly verified as the causal factor of human and mouse Parkinson's disease. However, biological function of α-SYN has not been clearly demonstrated until now. In this investigation, we reveal that α-SYN is a co-regulator of growth factor-induced AKT activation. Elimination of SYN reduces the IGF-1-mediated AKT activation. Similarly, mutant SYN suppresses the IGF-1-induced AKT activation. Wild-type SYN can interact with AKT and enhance the solubility
more » ... nce the solubility and plasma localization of AKT in response to IGF-1, whereas mutant α-SYNs do not interact with AKT. In addition, elevated expression of SYN blocks the AKT activation. We also find that si-RNA against α-SYN abolished the protective effect of IGF-1 against DNA damage-induced apoptosis. Our result strongly indicates that Parkinson's disease, induced by α-SYN mutation, is evoked by deregulation of the AKT-signaling cascade.
doi:10.6084/m9.figshare.5121766.v1 fatcat:hoe7hxhqp5gbbljm5afpxi32eu