Dishevelled Regulates the Metabolism of Amyloid Precursor Protein via Protein Kinase C/Mitogen-Activated Protein Kinase and c-Jun Terminal Kinase
作者： A. Mudher , S. Chapman , J. Richardson , A. Asuni , G. Gibb
DOI: 10.1523/JNEUROSCI.21-14-04987.2001
关键词:
摘要: Alzheimer's disease (AD) is a disorder of two pathologies: amyloid plaques, the core which peptide derived from precursor protein (APP), and neurofibrillary tangles composed highly phosphorylated tau. Protein kinase C (PKC) known to increase non-amyloidogenic alpha-secretase cleavage APP, producing secreted APP (sAPPalpha), glycogen synthase (GSK)-3beta tau phosphorylation. Both PKC GSK-3beta are components wnt signaling cascade. Here we demonstrate that overexpression another member this pathway, dishevelled (dvl-1), increases sAPPalpha production. The action on mediated via both c-jun terminal (JNK) (PKC)/mitogen-activated (MAP) but not p38 MAP kinase. These data position dvl-1 upstream JNK, thereby explaining previously observed dual dvl-1. Furthermore, show human wnt-1 also reduce phosphorylation by GSK-3beta. Therefore, metabolism potentially linked through signaling.
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