期刊
JOURNAL OF NEUROSCIENCE
卷 32, 期 11, 页码 3910-3916出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3916-11.2012
关键词
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资金
- University of Texas Medical Branch
- Whitehall Foundation
- National Natural Science Foundation of China [30873457]
- Scientific Technology Project of Guangdong Province of China [2008A060202010, 2010B050700019]
A disintegrin and metalloproteinase 10 (ADAM10) is the constitutive alpha-secretase that governs the nonamyloidogenic pathway of beta-amyloid precursor protein processing and is an attractive drug target for treating Alzheimer's disease. To date, little is known about the mechanism by which ADAM10 is regulated in neurons. Using mouse primary cortical neurons, we show here that NMDA receptor (NMDAR) activation led to upregulation of the genes encoding ADAM10 and beta-catenin proteins. Interestingly, the ADAM10 upregulation was abolished by inhibitors of Wnt/beta-catenin signaling. Conversely, activation of the Wnt/beta-catenin signaling pathway by recombinant Wnt3a stimulated ADAM10 expression. We further showed that both the NMDAR-and Wnt3a-induced ADAM10 upregulation was blocked by ERK inhibitors. We suggest that the NMDARs control ADAM10 expression via a Wnt/MAPK signaling pathway.
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