ArticleScience advances2022
RNF220 is an E3 ubiquitin ligase for AMPA receptors to regulate synaptic transmission.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 31 citations in OpenAlex.
- Transcriptomic analysis of spinal V1 interneurons informs their multifunctional role in motor output.Nature communications · 2026Article
- RNF220 safeguards meiotic synapsis and male fertility by antagonizing SYCE1 ubiquitination.Cell death & disease · 2026Article
- Human iPSC-Derived Mononuclear Phagocytes Improve Cognition and Neural Health across Multiple Mouse Models of Aging and Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Augmenting AMPA receptor signaling after spinal cord injury increases ependymal-derived neural stem/progenitor cell migration and promotes functional recovery.Nature neuroscience · 2025Article
- The pathogenic factor of ZC4H2-associated rare disorder is a postsynaptic regulator for synaptic activity and cognitive function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The autocrine motility factor receptor delays the pathological progression of Alzheimer's disease via regulating the ubiquitination-mediated degradation of APP.Alzheimer's research & therapy · 2025Article
- Oligodendrocytes and myelination: pioneering new frontiers in cognitive neuroscience.Frontiers in neuroscience · 2025Review
- Article
- Understanding neurodevelopmental proteasomopathies as new rare disease entities: A review of current concepts, molecular biomarkers, and perspectives.Genes & diseases · 2024Review
- The transcriptomic landscape of spinal V1 interneurons reveals a role for En1 in specific elements of motor output.bioRxiv : the preprint server for biology · 2024Article
- RNF220-mediated K63-linked polyubiquitination stabilizes Olig proteins during oligodendroglial development and myelination.Science advances · 2024Article
- Involvement of ubiquitination in Alzheimer's disease.Frontiers in neurology · 2024Review
- Molecular Mechanisms of AMPA Receptor Trafficking in the Nervous System.International journal of molecular sciences · 2023Review
- MEX3C induces cognitive impairment in mice through autophagy inhibition.Brain and behavior · 2023Article
- Molecular Pathogenic Mechanisms of Hypomyelinating Leukodystrophies (HLDs).Neurology international · 2023Review
- Ubiquitination of the GluA1 Subunit of AMPA Receptors Is Required for Synaptic Plasticity, Memory, and Cognitive Flexibility.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The accurate expression of postsynaptic AMPA receptors (AMPARs) is critical for information processing in the brain, and ubiquitination is a key regulator for this biological process. However, the roles of E3 ubiquitin ligases in the regulation of AMPARs are poorly understood. Here, we find that RNF220 directly interacts with AMPARs to meditate their polyubiquitination, and RNF220 knockout specifically increases AMPAR protein levels, thereby enhancing basal synaptic activity while impairing synaptic plasticity. Moreover, depending on its E3 ubiquitin ligase activity, RNF220 represses AMPAR-mediated excitatory synaptic responses and their neuronal surface expression. Furthermore, learning and memory are altered in forebrain RNF220-deficient mice. In addition, two neuropathology-related RNF220 variants fail to repress excitatory synaptic activity because of the incapability to regulate AMPAR ubiquitination due to their attenuated interaction. Together, we identify RNF220 as an E3 ubiquitin ligase for AMPARs and establish its substantial role in excitatory synaptic transmission and brain function.
Identifiers
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.