ArticleeLife2017
The E3 ubiquitin ligase IDOL regulates synaptic ApoER2 levels and is important for plasticity and learning.
Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Review
- Deletion of neuronal Idol ameliorates Alzheimer's disease-related pathologies via APOE receptors.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The selenoprotein P/ApoER2 axis facilitates selenium accumulation in selenoprotein P-accepting cells and confers prolonged resistance to ferroptosis.Redox biology · 2025Article
- MYLIP attenuates hypoxia tolerance by inducing K27-linked polyubiquitination and subsequent proteasomal degradation of HIF-α.Communications biology · 2025Article
- Arachidonic Acid Mobilization and Peroxidation Promote Microglial Dysfunction in Aβ Pathology.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Review
- MEX3C induces cognitive impairment in mice through autophagy inhibition.Brain and behavior · 2023Article
- Liver X Receptor-Inducible Host E3 Ligase IDOL Targets a Human Cytomegalovirus Reactivation Determinant.Journal of virology · 2023Article
- High-Sensitivity Intrinsic Optical Signal Imaging Through Flexible, Low-Cost Adaptations of an Upright Microscope.eNeuro · 2023Article
- ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease.Neurobiology of aging · 2022Review
- Activity-regulated E3 ubiquitin ligase TRIM47 modulates excitatory synapse development.Frontiers in molecular neuroscience · 2022Article
- Historical perspective and progress on protein ubiquitination at glutamatergic synapses.Neuropharmacology · 2021Review
- Barrel cortex plasticity after photothrombotic stroke involves potentiating responses of pre-existing circuits but not functional remapping to new circuits.Nature communications · 2021Article
- Blocking the Spinal Fbxo3/CARM1/KNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Structural analysis of the LDL receptor-interacting FERM domain in the E3 ubiquitin ligase IDOL reveals an obscured substrate-binding site.The Journal of biological chemistry · 2020Article
- Reelin Functions, Mechanisms of Action and Signaling Pathways During Brain Development and Maturation.Biomolecules · 2020Review
- Therapeutic IDOL Reduction Ameliorates Amyloidosis and Improves Cognitive Function in APP/PS1 Mice.Molecular and cellular biology · 2020Article
- ApoER2: Functional Tuning Through Splicing.Frontiers in molecular neuroscience · 2020Review
- The Reelin Receptors Apolipoprotein E receptor 2 (ApoER2) and VLDL Receptor.International journal of molecular sciences · 2018Review
- Inactivation of the E3 Ubiquitin Ligase IDOL Attenuates Diet-Induced Obesity and Metabolic Dysfunction in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Neuronal ApoE receptors are linked to learning and memory, but the pathways governing their abundance, and the mechanisms by which they affect the function of neural circuits are incompletely understood. Here we demonstrate that the E3 ubiquitin ligase IDOL determines synaptic ApoER2 protein levels in response to neuronal activation and regulates dendritic spine morphogenesis and plasticity. IDOL-dependent changes in ApoER2 abundance modulate dendritic filopodia initiation and synapse maturation. Loss of IDOL in neurons results in constitutive overexpression of ApoER2 and is associated with impaired activity-dependent structural remodeling of spines and defective LTP in primary neuron cultures and hippocampal slices. IDOL-deficient mice show profound impairment in experience-dependent reorganization of synaptic circuits in the barrel cortex, as well as diminished spatial and associative learning. These results identify control of lipoprotein receptor abundance by IDOL as a post-transcriptional mechanism underlying the structural and functional plasticity of synapses and neural circuits.
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What 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.