ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
The amyloid precursor protein interacts with Go heterotrimeric protein within a cell compartment specialized in signal transduction.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
32 citing papers in PubMed, 101 citations in OpenAlex.
- Structural biology of cell surface receptors implicated in Alzheimer's disease.Biophysical reviews · 2022Review
- Aβ Assemblies Promote Amyloidogenic Processing of APP and Intracellular Accumulation of Aβ42 Through Go/Gβγ Signaling.Frontiers in cell and developmental biology · 2022Article
- Soluble Amyloid Precursor Protein Alpha Interacts with alpha3-Na, K-ATPAse to Induce Axonal Outgrowth but Not Neuroprotection: Evidence for Distinct Mechanisms Underlying these Properties.Molecular neurobiology · 2018Article
- Amyloid Precursor Protein family as unconventional Go-coupled receptors and the control of neuronal motility.Neurogenesis (Austin, Tex.) · 2017Review
- Role of APP Interactions with Heterotrimeric G Proteins: Physiological Functions and Pathological Consequences.Frontiers in molecular neuroscience · 2017Review
- Amyloid precursor protein modulates Nav1.6 sodium channel currents through a Go-coupled JNK pathway.Scientific reports · 2016Article
- Manduca Contactin Regulates Amyloid Precursor Protein-Dependent Neuronal Migration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- APP Receptor? To Be or Not To Be.Trends in pharmacological sciences · 2016Review
- Amyloid Precursor Proteins Are Dynamically Trafficked and Processed during Neuronal Development.Frontiers in molecular neuroscience · 2016Article
- Amyloid precursor protein enhances Nav1.6 sodium channel cell surface expression.The Journal of biological chemistry · 2015Article
- PAT1 inversely regulates the surface Amyloid Precursor Protein level in mouse primary neurons.BMC neuroscience · 2015Article
- Amyloid precursor protein interaction network in human testis: sentinel proteins for male reproduction.BMC bioinformatics · 2015Article
- Lipid rafts in neurodegeneration and neuroprotection.Molecular neurobiology · 2014Review
- Amyloid β precursor protein as a molecular target for amyloid β--induced neuronal degeneration in Alzheimer's disease.Neurobiology of aging · 2013Review
- Citrulline diet supplementation improves specific age-related raft changes in wild-type rodent hippocampus.Age (Dordrecht, Netherlands) · 2013Article
- Amyloid precursor proteins interact with the heterotrimeric G protein Go in the control of neuronal migration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Novel GαS-protein signaling associated with membrane-tethered amyloid precursor protein intracellular domain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Neurodegeneration in Alzheimer disease: role of amyloid precursor protein and presenilin 1 intracellular signaling.Journal of toxicology · 2012Article
- Deregulated sphingolipid metabolism and membrane organization in neurodegenerative disorders.Molecular neurobiology · 2010Review
- Interactions between the amyloid precursor protein C-terminal domain and G proteins mediate calcium dysregulation and amyloid beta toxicity in Alzheimer's disease.The FEBS journal · 2009Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The function of the beta-amyloid protein precursor (betaAPP), a transmembrane molecule involved in Alzheimer pathologies, is poorly understood. We recently reported the presence of a fraction of betaAPP in cholesterol and sphingoglycolipid-enriched microdomains (CSEM), a caveolae-like compartment specialized in signal transduction. To investigate whether betaAPP actually interferes with cell signaling, we reexamined the interaction between betaAPP and Go GTPase. In strong contrast with results obtained with reconstituted phospholipid vesicles (Okamoto et al., 1995), we find that incubating total neuronal membranes with 22C11, an antibody that recognizes an N-terminal betaAPP epitope, reduces high-affinity Go GTPase activity. This inhibition is specific of Galphao and is reproduced, in the absence of 22C11, by the addition of the betaAPP C-terminal domain but not by two distinct mutated betaAPP C-terminal domains that do not bind Galphao. This inhibition of Galphao GTPase activity by either 22C11 or wild-type betaAPP cytoplasmic domain suggests that intracellular interactions between betaAPP and Galphao could be regulated by extracellular signals. To verify whether this interaction is preserved in CSEM, we first used biochemical, immunocytochemical, and ultrastructural techniques to unambiguously confirm the colocalization of Galphao and betaAPP in CSEM. We show that inhibition of basal Galphao GTPase activity also occurs within CSEM and correlates with the coimmunoprecipitation of Galphao and betaAPP. The regulation of Galphao GTPase activity by betaAPP in a compartment specialized in signaling may have important consequences for our understanding of the physiopathological functions of betaAPP.
Indexed as
Identifiers
10024358PMC6782156W2161335932What 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.