AMPK interacts with DSCAM and plays an important role in netrin-1 induced neurite outgrowth.
10.1007/s13238-012-2126-2
- Author:
Kun ZHU
1
;
Xiaoping CHEN
;
Jianghong LIU
;
Haihong YE
;
Li ZHU
;
Jane Y WU
Author Information
1. State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
- Publication Type:Journal Article
- MeSH:
AMP-Activated Protein Kinases;
antagonists & inhibitors;
genetics;
metabolism;
Animals;
Cell Adhesion Molecules;
genetics;
metabolism;
Cells, Cultured;
HEK293 Cells;
Humans;
Mice;
Nerve Growth Factors;
pharmacology;
Netrin-1;
Neurites;
physiology;
Neurons;
cytology;
drug effects;
metabolism;
Phosphorylation;
Protein Binding;
Protein Kinase Inhibitors;
pharmacology;
RNA Interference;
RNA, Small Interfering;
Recombinant Fusion Proteins;
biosynthesis;
genetics;
Signal Transduction;
drug effects;
Transfection;
Tumor Suppressor Proteins;
pharmacology
- From:
Protein & Cell
2013;4(2):155-161
- CountryChina
- Language:English
-
Abstract:
Down syndrome cell adhesion molecule (DSCAM) acts as a netrin-1 receptor and mediates attractive response of axons to netrin-1 in neural development. However, the signaling mechanisms of netrin-DSCAM remain unclear. Here we report that AMP-activated protein kinase (AMPK) interacts with DSCAM through its γ subunit, but does not interact with DCC (deleted in colorectal cancer), another major receptor for netrin-1. Netrin-treatment of cultured cortical neurons leads to increased phosphorylation of AMPK. Both AMPK mutant with dominant-negative effect and AMPK inhibitor can significantly suppress netrin-1 induced neurite outgrowth. Together, these findings demonstrate that AMPK interacts with DSCAM and plays an important role in netrin-1 induced neurite outgrowth. Our study uncovers a previously unknown component, AMPK, in netrin-DSCAM signaling pathway.
