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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Acknowledgments
We thank Dr. J. L. Noebels (Baylor College of Medicine) for providing pcDNA3.1-LGI3-myc. This research was supported by the Chung-Ang University Research Grants in 2010.
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Park, WJ., Lim, Y.Y., Kwon, N.S. et al. Leucine-Rich Glioma Inactivated 3 Induces Neurite Outgrowth Through Akt and Focal Adhesion Kinase. Neurochem Res 35, 789–796 (2010). https://doi.org/10.1007/s11064-010-0136-0
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DOI: https://doi.org/10.1007/s11064-010-0136-0