ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Regulation of amyloid precursor protein catabolism involves the mitogen-activated protein kinase signal transduction pathway.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 132 citations in OpenAlex.
- Review
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- Role of Receptors in Relation to Plaques and Tangles in Alzheimer's Disease Pathology.International journal of molecular sciences · 2021Review
- APP Binds to the EGFR Ligands HB-EGF and EGF, Acting Synergistically with EGF to Promote ERK Signaling and Neuritogenesis.Molecular neurobiology · 2021Article
- Role of amyloid β protein receptors in mediating synaptic plasticity.Biomedical reports · 2017Article
- Oxidative stress affects processing of amyloid precursor protein in vascular endothelial cells.PloS one · 2017Article
- The calcineurin inhibitor Sarah (Nebula) exacerbates Aβ42 phenotypes in a Drosophila model of Alzheimer's disease.Disease models & mechanisms · 2016Article
- Synaptic therapy in Alzheimer's disease: a CREB-centric approach.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015Review
- AMPA receptor activation promotes non-amyloidogenic amyloid precursor protein processing and suppresses neuronal amyloid-β production.PloS one · 2013Article
- Link between cancer and Alzheimer disease via oxidative stress induced by nitric oxide-dependent mitochondrial DNA overproliferation and deletion.Oxidative medicine and cellular longevity · 2013Review
- Dissociation of ERK signalling inhibition from the anti-amyloidogenic action of synthetic ceramide analogues.Clinical science (London, England : 1979) · 2012Article
- Obesity, leptin, and Alzheimer's disease.Annals of the New York Academy of Sciences · 2011Review
- Serotonin signaling is associated with lower amyloid-β levels and plaques in transgenic mice and humans.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- The role of G protein-coupled receptors in the pathology of Alzheimer's disease.Nature reviews. Neuroscience · 2011Review
- Protein kinase C-regulated aβ production and clearance.International journal of Alzheimer's disease · 2011Article
- TRPM7 activates m-calpain by stress-dependent stimulation of p38 MAPK and c-Jun N-terminal kinase.Journal of molecular biology · 2010Article
- Interleukin-1beta enhances nucleotide-induced and alpha-secretase-dependent amyloid precursor protein processing in rat primary cortical neurons via up-regulation of the P2Y(2) receptor.Journal of neurochemistry · 2009Article
- S100A7, a novel Alzheimer's disease biomarker with non-amyloidogenic alpha-secretase activity acts via selective promotion of ADAM-10.PloS one · 2009Article
- Progesterone increases brain-derived neuroptrophic factor expression and protects against glutamate toxicity in a mitogen-activated protein kinase- and phosphoinositide-3 kinase-dependent manner in cerebral cortical explants.Journal of neuroscience research · 2007Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Catabolic processing of the amyloid precursor protein (APP) is subject to regulatory control by protein kinases. We hypothesized that this regulation involves sequential activation of the enzymes mitogen-activated protein kinase kinase (MEK) and extracellular signal-regulated protein kinase (ERK). In the present investigation, we provide evidence that MEK is critically involved in regulating APP processing by both nerve growth factor and phorbol esters. Western blot analysis of the soluble N-terminal APP derivative APPs demonstrated that the synthetic MEK inhibitor PD 98059 antagonized nerve growth factor stimulation of both APPs production and ERK activation in PC12 cells. Moreover, PD 98059 inhibited phorbol ester stimulation of APPs production and activation of ERK in both human embryonic kidney cells and cortical neurons. Furthermore, overexpression of a kinase-inactive MEK mutant inhibited phorbol ester stimulation of APP secretion and activation of ERK in human embryonic kidney cell lines. Most important, PD 98059 antagonized phorbol ester-mediated inhibition of Abeta secretion from cells overexpressing human APP695 carrying the "Swedish mutation." Taken together, these data indicate that MEK and ERK may be critically involved in protein kinase C and nerve growth factor regulation of APP processing. The mitogen-activated protein kinase cascade may provide a novel target for altering catabolic processing of APP.
Indexed as
Identifiers
9390997PMC6573401W1794943105What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.