ArticleThe Journal of biological chemistry2008
Dexras1 interacts with FE65 to regulate FE65-amyloid precursor protein-dependent transcription.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 55 citations in OpenAlex.
- Pan-Cancer Analysis Identifies a Ras-Related GTPase as a Potential Modulator of Cancer.International journal of molecular sciences · 2025Article
- PTMint database of experimentally verified PTM regulation on protein-protein interaction.Bioinformatics (Oxford, England) · 2023Article
- ARNO is recruited by the neuronal adaptor FE65 to potentiate ARF6-mediated neurite outgrowth.Open biology · 2022Article
- Affinity Proteomics Identifies Interaction Partners and Defines Novel Insights into the Function of the Adhesion GPCR VLGR1/ADGRV1.Molecules (Basel, Switzerland) · 2022Article
- Fe65: A Scaffolding Protein of Actin Regulators.Cells · 2021Review
- Attenuation of amyloid-β generation by atypical protein kinase C-mediated phosphorylation of engulfment adaptor PTB domain containing 1 threonine 35.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Amyloid Precursor Protein Is Associated with Aggressive Behavior in Nonluminal Breast Cancers.The oncologist · 2018Article
- Planar cell polarity geneEMBO reports · 2018Article
- Neuronal adaptor FE65 stimulates Rac1-mediated neurite outgrowth by recruiting and activating ELMO1.The Journal of biological chemistry · 2018Article
- A peptidylic inhibitor for neutralizing expandedRNA (New York, N.Y.) · 2018Article
- P2X receptor overexpression induced by soluble oligomers of amyloid beta peptide potentiates synaptic failure and neuronal dyshomeostasis in cellular models of Alzheimer's disease.Neuropharmacology · 2018Article
- Phosphorylation of FE65 at threonine 579 by GSK3β stimulates amyloid precursor protein processing.Scientific reports · 2017Article
- A brain-targeting lipidated peptide for neutralizing RNA-mediated toxicity in Polyglutamine Diseases.Scientific reports · 2017Article
- FE65 and FE65L1 share common synaptic functions and genetically interact with the APP family in neuromuscular junction formation.Scientific reports · 2016Article
- Assessing a peptidylic inhibitor-based therapeutic approach that simultaneously suppresses polyglutamine RNA- and protein-mediated toxicities in patient cells and Drosophila.Disease models & mechanisms · 2016Article
- Immununochemical Markers of the Amyloid Cascade in the Hippocampus in Motor Neuron Diseases.Frontiers in neurology · 2016Article
- Article
- Phosphorylation of FE65 Ser610 by serum- and glucocorticoid-induced kinase 1 modulates Alzheimer's disease amyloid precursor protein processing.The Biochemical journal · 2015Article
- FE65 interacts with ADP-ribosylation factor 6 to promote neurite outgrowth.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Neprilysin and Aβ Clearance: Impact of the APP Intracellular Domain in NEP Regulation and Implications in Alzheimer's Disease.Frontiers in aging neuroscience · 2013Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 4 countries.
Funding
Abstract
FE65 is an adaptor protein that binds to and forms a transcriptionally active complex with the gamma-secretase-derived amyloid precursor protein (APP) intracellular domain. The regulatory mechanisms of FE65-APP-mediated transcription are still not clear. In this report, we demonstrate that Dexras1, a Ras family small G protein, binds to FE65 PTB2 domain and potently suppresses the FE65-APP-mediated transcription. The suppression is not via competition for binding of FE65 between Dexras1 and APP because the two proteins can simultaneously bind to the FE65 PTB2 domain. Phosphorylation of FE65 tyrosine 547 within the PTB2 domain has been shown to enhance FE65-APP-mediated transcription but not to influence binding to APP. Here we find that this phosphorylation event reduces the binding between Dexras1 and FE65. We also demonstrate that Dexras1 inhibits the FE65-APP-mediated transcription of glycogen synthase kinase 3beta (GSK3 beta). Moreover, small interfering RNA knockdown of Dexras1 enhances GSK3 beta expression and increases phosphorylation of Tau, a GSK3 beta substrate. Thus, Dexras1 functions as a suppressor of FE65-APP-mediated transcription, and FE65 tyrosine 547 phosphorylation enhances FE65-APP-mediated transcription, at least in part, by modulating the interaction between FE65 and Dexras1. These findings reveal a novel regulatory mechanism for FE65-APP-mediated 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.