Leucine-Rich Glioma Inactivated 3 Induces Neurite Outgrowth Through Akt and Focal Adhesion Kinase

被引:28
作者
Park, Woo-Jae [1 ]
Lim, Yun Young [2 ]
Kwon, Nyoun Soo [1 ]
Baek, Kwang Jin [1 ]
Kim, Dong-Seok [1 ]
Yun, Hye-Young [1 ]
机构
[1] Chung Ang Univ, Coll Med, Dept Biochem, Seoul 156756, South Korea
[2] Chung Ang Univ, Coll Med, Dept Dermatol, Seoul 156756, South Korea
关键词
LGI3; Neurite; Akt; FAK; Phosphorylation; Differentiation; LGI1; GENE; EPILEPSY; MUTATIONS; REPEAT; BRAIN; ASTROCYTES; PROTEINS; GROWTH; 10Q24; FAK;
D O I
10.1007/s11064-010-0136-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:789 / 796
页数:8
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