Journal
PROTEIN & CELL
Volume 4, Issue 2, Pages 155-161Publisher
HIGHER EDUCATION PRESS
DOI: 10.1007/s13238-012-2126-2
Keywords
AMP-activated protein kinase (AMPK); neurite outgrowth; Down syndrome cell adhesion molecule (DSCAM); netrin
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Funding
- National Basic Research Program (973 Program) [2010CB529603, 2009CB825402]
- National Natural Science Foundation of China [91132710]
- Chinese Academy of Science (CASNN-GWPPS)
- NIH [RO1AG033004, R56NS074763]
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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 gamma 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.
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