ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
FE65 interacts with ADP-ribosylation factor 6 to promote neurite outgrowth.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Autism spectrum disorder-associated Sema5A p.Arg676Cys drives Arf6/FE65 signaling and aberrant cell morphogenesis.Scientific reports · 2026Article
- Small GTPases control macropinocytosis of amyloid precursor protein and cleavage to amyloid-β.Heliyon · 2024Article
- Discovery and validation of PURA as a transcription target of 20(S)-protopanaxadiol: Implications for the treatment of cognitive dysfunction.Journal of ginseng research · 2023Article
- Amyloid precursor protein and its interacting proteins in neurodevelopment.Biochemical Society transactions · 2023Review
- ARNO is recruited by the neuronal adaptor FE65 to potentiate ARF6-mediated neurite outgrowth.Open biology · 2022Article
- Physiological and Pathological Roles of the Cytohesin Family in Neurons.International journal of molecular sciences · 2022Review
- 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
- Regulation of Neurotransmitter Release by Amyloid Precursor Protein Through Synapsin Phosphorylation.Neurochemical research · 2019Article
- Emerging roles of the neural adaptor FE65 in neurite outgrowth.Neural regeneration research · 2018Article
- Neuronal adaptor FE65 stimulates Rac1-mediated neurite outgrowth by recruiting and activating ELMO1.The Journal of biological chemistry · 2018Article
- GULP1/CED-6 ameliorates amyloid-β toxicity in a Drosophila model of Alzheimer's disease.Oncotarget · 2017Article
- Phosphorylation of FE65 at threonine 579 by GSK3β stimulates amyloid precursor protein processing.Scientific reports · 2017Article
- Not just amyloid: physiological functions of the amyloid precursor protein family.Nature reviews. Neuroscience · 2017Review
- SRRM4-dependent neuron-specific alternative splicing of protrudin transcripts regulates neurite outgrowth.Scientific reports · 2017Article
- APP Protein Family Signaling at the Synapse: Insights from Intracellular APP-Binding Proteins.Frontiers in molecular neuroscience · 2017Review
- FE65 and FE65L1 share common synaptic functions and genetically interact with the APP family in neuromuscular junction formation.Scientific reports · 2016Article
- Arf6 controls beta-amyloid production by regulating macropinocytosis of the Amyloid Precursor Protein to lysosomes.Molecular brain · 2015Article
- FE65 and FE65L1 amyloid precursor protein-binding protein compound null mice display adult-onset cataract and muscle weakness.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Regulation of neuronal survival and morphology by the E3 ubiquitin ligase RNF157.Cell death and differentiation · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
FE65 is an adaptor protein that binds to the amyloid precursor protein (APP). As such, FE65 has been implicated in the pathogenesis of Alzheimer's disease. In addition, evidence suggests that FE65 is involved in brain development. It is generally believed that FE65 participates in these processes by recruiting various interacting partners to form functional complexes. Here, we show that via its first phosphotyrosine binding (PTB) domain, FE65 binds to the small GTPase ADP-ribosylation factor 6 (ARF6). FE65 preferentially binds to ARF6-GDP, and they colocalize in neuronal growth cones. Interestingly, FE65 stimulates the activation of both ARF6 and its downstream GTPase Rac1, a regulator of actin dynamics, and functions in growth cones to stimulate neurite outgrowth. We show that transfection of FE65 and/or ARF6 promotes whereas small interfering RNA knockdown of FE65 or ARF6 inhibits neurite outgrowth in cultured neurons as compared to the mock-transfected control cells. Moreover, knockdown of ARF6 attenuates FE65 stimulation of neurite outgrowth and defective neurite outgrowth seen in FE65-deficient neurons is partially corrected by ARF6 overexpression. Notably, the stimulatory effect of FE65 and ARF6 on neurite outgrowth is abrogated either by dominant-negative Rac1 or knockdown of Rac1. Thus, we identify FE65 as a novel regulator of neurite outgrowth via controlling ARF6-Rac1 signaling.
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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.