Direct Interaction of alpha-Synuclein and AKT Regulates IGF-1 Signaling: Implication of Parkinson Disease
- Authors
- Chung, Ji-Yun; Lee, Su-Jin; Lee, Sun-Hye; Jung, Youn Sang; Ha, Nam-Chul; Seol, Wongi; Park, Bum-Joon
- Issue Date
- Jun-2011
- Publisher
- KARGER
- Keywords
- alpha-Synuclein; AKT; Parkinson's disease; IGF-1 signaling
- Citation
- NEUROSIGNALS, v.19, no.2, pp 86 - 96
- Pages
- 11
- Journal Title
- NEUROSIGNALS
- Volume
- 19
- Number
- 2
- Start Page
- 86
- End Page
- 96
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/65019
- DOI
- 10.1159/000325028
- ISSN
- 1424-862X
1424-8638
- Abstract
- Genetic mutation of alpha-synuclein (alpha-SYN) is clearly verified as the causal factor of human and mouse Parkinson's disease. However, biological function of alpha-SYN has not been clearly demonstrated until now. In this investigation, we reveal that alpha-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 and plasma localization of AKT in response to IGF-1, whereas mutant alpha-SYNs do not interact with AKT. In addition, elevated expression of SYN blocks the AKT activation. We also find that si-RNA against alpha-SYN abolished the protective effect of IGF-1 against DNA damage-induced apoptosis. Our result strongly indicates that Parkinson's disease, induced by alpha-SYN mutation, is evoked by deregulation of the AKT-signaling cascade. Copyright (C) 2011 S. Karger AG, Basel
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Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
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