ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
The amyloid precursor protein and its regulatory protein, FE65, in growth cones and synapses in vitro and in vivo.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
80 citing papers in PubMed, 178 citations in OpenAlex.
- Article
- Development of a brain-penetrant G9a methylase inhibitor to target Alzheimer's disease-associated proteopathology.Nature communications · 2025Article
- Therapeutic and preventive strategies based on the maladaptive plasticity hypothesis for Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- FE65: a hub for neurodevelopment.Neural regeneration research · 2024Article
- The Drosophila homolog of APP promotes Dscam expression to drive axon terminal growth, revealing interaction between Down syndrome genes.Disease models & mechanisms · 2023Article
- Reelin and APP Cooperatively Modulate Dendritic Spine FormationExperimental neurobiology · 2023Article
- Review
- Examination of Longitudinal Alterations in Alzheimer's Disease-Related Neurogenesis in an APP/PS1 Transgenic Mouse Model, and the Effects of P33, a Putative Neuroprotective Agent Thereon.International journal of molecular sciences · 2022Article
- Downregulation of PIK3CB Involved in Alzheimer's Disease via Apoptosis, Axon Guidance, and FoxO Signaling Pathway.Oxidative medicine and cellular longevity · 2022Article
- Signaling abnormality leading to excessive/aberrant synaptic plasticity in Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- The Amyloid Forming Peptides Islet Amyloid Polypeptide and Amyloid β Interact at the Molecular Level.International journal of molecular sciences · 2021Article
- GSAP regulates lipid homeostasis and mitochondrial function associated with Alzheimer's disease.The Journal of experimental medicine · 2021Article
- Fe65: A Scaffolding Protein of Actin Regulators.Cells · 2021Review
- Genetically Encoded Calcium Indicators Can Impair Dendrite Growth of Cortical Neurons.Frontiers in cellular neuroscience · 2020Article
- Effects of the Pentapeptide P33 on Memory and Synaptic Plasticity in APP/PS1 Transgenic Mice: A Novel Mechanism Presenting the Protein Fe65 as a Target.International journal of molecular sciences · 2019Article
- Regulation of Neurotransmitter Release by Amyloid Precursor Protein Through Synapsin Phosphorylation.Neurochemical research · 2019Article
- Early and reversible changes to the hippocampal proteome in mice on a high-fat diet.Nutrition & metabolism · 2019Article
- Neuronal adaptor FE65 stimulates Rac1-mediated neurite outgrowth by recruiting and activating ELMO1.The Journal of biological chemistry · 2018Article
- Not just amyloid: physiological functions of the amyloid precursor protein family.Nature reviews. Neuroscience · 2017Review
- APP Protein Family Signaling at the Synapse: Insights from Intracellular APP-Binding Proteins.Frontiers in molecular neuroscience · 2017Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Although the Alzheimer amyloid protein precursor (APP) has been studied intensely for more than a decade, its function in neurons is unresolved. Much less is known about its binding partner FE65. We have shown recently that APP and FE65 synergistically regulate the movement of transfected cells. It remained to be shown whether endogenous APP and FE65 could play a similar role in vivo. Here, we show that FE65, like APP, is expressed at high levels in neurons. Using a combination of immunofluorescence, live imaging, and subcellular fractionation, we find that FE65 and APP localize in vitro and in vivo to the most motile regions of neurons, the growth cones. Within growth cones, APP and FE65 concentrate in actin-rich lamellipodia. Finally, APP and FE65 interact in nerve terminals, where they associate with Rab5-containing synaptic organelles but not with synaptic vesicles. Our data are consistent with a role for the APP/FE65 complex in regulation of actin-based membrane motility in neurons, which could be important for highly dynamic processes such as neurite growth and synapse modification.
Indexed as
Identifiers
12843239PMC6741254W1684032030What 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.