Leucine-Rich Glioma Inactivated 3 Induces Neurite Outgrowth Through Akt and Focal Adhesion Kinase
- Authors
- Park, Woo-Jae; Lim, Yun Young; Kwon, Nyoun Soo; Baek, Kwang Jin; Kim, Dong-Seok; Yun, Hye-Young
- Issue Date
- May-2010
- Publisher
- SPRINGER/PLENUM PUBLISHERS
- Keywords
- LGI3; Neurite; Akt; FAK; Phosphorylation; Differentiation
- Citation
- NEUROCHEMICAL RESEARCH, v.35, no.5, pp 789 - 796
- Pages
- 8
- Journal Title
- NEUROCHEMICAL RESEARCH
- Volume
- 35
- Number
- 5
- Start Page
- 789
- End Page
- 796
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/22469
- DOI
- 10.1007/s11064-010-0136-0
- ISSN
- 0364-3190
1573-6903
- Abstract
- Leucine-rich glioma inactivated 3 (LGI3) is a secreted protein that belongs to LGI/epitempin family. LGI3 is highly expressed in brain in a transcriptionally and developmentally regulated manner. Here we found that LGI3 induced neurite outgrowth in Neuro-2a cells and dorsal root ganglia explants. LGI3 treatment or overexpression increased neurite outgrowth and knockdown of LGI3 by siRNA had opposite effect. LGI3 treatment increased phosphorylation of Akt and a 125-kDa protein. Immunoprecipitation identified the 125-kDa protein as focal adhesion kinase (FAK). LGI3 overexpression increased phospho-Akt, phospho-FAK and FAK protein. Inhibition of Akt activation by PI3 kinase inhibitor attenuated LGI3-induced FAK phosphorylation and neurite outgrowth. Taken together, we propose that LGI3 is a neuritogenic factor whose signaling pathway involves Akt-mediated FAK activation.
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Collections - College of Medicine > College of Medicine > 1. Journal Articles
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