期刊
SCIENCE
卷 323, 期 5916, 页码 946-951出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1160649
关键词
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资金
- Methusalem grant from the Flemish government [IWT990363, IWT010512, IWT030623]
- Fund for Scientific Research (Flanders, Belgium)
- Federal Office for Scientific Affairs, Belgium [IUAP P6/43/]
Deposition of the amyloid-beta peptide is a pathological hallmark of Alzheimer's disease. A high- throughput functional genomics screen identified G protein- coupled receptor 3 ( GPR3), a constitutively active orphan G protein- coupled receptor, as a modulator of amyloid-beta production. Overexpression of GPR3 stimulated amyloid-beta production, whereas genetic ablation of GPR3 prevented accumulation of the amyloid-beta peptide in vitro and in an Alzheimer's disease mouse model. GPR3 expression led to increased formation and cell- surface localization of the mature gamma-secretase complex in the absence of an effect on Notch processing. GPR3 is highly expressed in areas of the normal human brain implicated in Alzheimer's disease and is elevated in the sporadic Alzheimer's disease brain. Thus, GPR3 represents a potential therapeutic target for the treatment of Alzheimer's disease.
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