ArticleScientific reports2016
FE65 and FE65L1 share common synaptic functions and genetically interact with the APP family in neuromuscular junction formation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Gene-Exercise Interactions in Amyloid Metabolism and Clearance: Implications for Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Essential Regulation of Spermatogonial Stem Cell Fate Decisions and Male Fertility by APBB1 via Interaction with KAT5 and GDF15 in Humans and Mice.Research (Washington, D.C.) · 2025Article
- The AICD interactome: implications in neurodevelopment and neurodegeneration.Biochemical Society transactions · 2024Review
- FE65: a hub for neurodevelopment.Neural regeneration research · 2024Article
- Amyloid precursor protein and its interacting proteins in neurodevelopment.Biochemical Society transactions · 2023Review
- Direct electrical stimulation impacts on neuromuscular junction morphology on both stimulated and unstimulated contralateral soleus.Journal of cachexia, sarcopenia and muscle · 2023Article
- FE65 in breast cancer and its clinicopathological significance.Breast cancer (Tokyo, Japan) · 2022Article
- Fe65: A Scaffolding Protein of Actin Regulators.Cells · 2021Review
- Amyloid, APP, and Electrical Activity of the Brain.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2020Review
- Genetically Encoded Calcium Indicators Can Impair Dendrite Growth of Cortical Neurons.Frontiers in cellular neuroscience · 2020Article
- 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
- Functional Roles of the Interaction of APP and Lipoprotein Receptors.Frontiers in molecular neuroscience · 2017Review
- Fe65-PTB2 Dimerization Mimics Fe65-APP Interaction.Frontiers in molecular neuroscience · 2017Article
- APP Protein Family Signaling at the Synapse: Insights from Intracellular APP-Binding Proteins.Frontiers in molecular neuroscience · 2017Review
- Novel Insights into the Physiological Function of the APP (Gene) Family and Its Proteolytic Fragments in Synaptic Plasticity.Frontiers in molecular neuroscience · 2016Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
The FE65 adaptor proteins (FE65, FE65L1 and FE65L2) bind proteins that function in diverse cellular pathways and are essential for specific biological processes. Mice lacking both FE65 and FE65L1 exhibit ectopic neuronal positioning in the cortex and muscle weakness. p97FE65-KO mice, expressing a shorter FE65 isoform able to bind amyloid precursor protein family members (APP, APLP1, APLP2), develop defective long-term potentiation (LTP) and aged mice display spatial learning and memory deficits that are absent from young mice. Here, we examined the central and peripheral nervous systems of FE65-KO, FE65L1-KO and FE65/FE65L1-DKO mice. We find spatial learning and memory deficits in FE65-KO and FE65L1-KO mice. Severe motor impairments, anxiety, hippocampal LTP deficits and neuromuscular junction (NMJ) abnormalities, characterized by decreased size and reduced apposition of pre- and postsynaptic sites, are observed in FE65/FE65L1-DKO mice. As their NMJ deficits resemble those of mutant APP/APLP2-DKO mice lacking the FE65/FE65L1 binding site, the NMJs of APLP2/FE65-DKO and APLP2/FE65L1-DKO mice were analyzed. NMJ deficits are aggravated in these mice when compared to single FE65- and FE65L1-KO mice. Together, our data demonstrate a role for FE65 proteins at central and peripheral synapses possibly occurring downstream of cell surface-associated APP/APLPs.
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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.