ReviewJournal of neurochemistry2016
Perturbed proteostasis in autism spectrum disorders.
Review in Journal of neurochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 78 citations in OpenAlex.
- Translational dysregulation as a mechanistic driver of cognitive, behavioral, and affective phenotypes in FXS and TSC.Neuroscience and biobehavioral reviews · 2026Review
- Review
- ASD mutations in the ciliary gene CEP41 impact development of projection neurons and interneurons in a human cortical organoid model.Molecular psychiatry · 2026Article
- Impaired Activity-Regulated Proteostasis: A Shared Mechanism in Neurodevelopmental Disorders.Biological psychiatry · 2026Review
- Correction of eIF4E overactivation rescues translatome imbalance and core ASD-like behaviors in valproic acid-induced offspring mice.Molecular psychiatry · 2026Article
- The E3 Ubiquitin Ligase UBE3B Regulates Synaptic Development and Cortical Network Activity.Autism research : official journal of the International Society for Autism Research · 2026Article
- Protein trafficking and synaptic demand configure complex and dynamic synaptome architectures of individual neurons.Scientific reports · 2026Article
- Extracellular vesicle profiling reveals novel autism signatures in patient-derived forebrain organoids.Translational psychiatry · 2025Article
- Bridging molecular and cellular neuroscience with proximity labeling technologies.Experimental & molecular medicine · 2025Review
- Construction destruction: Contribution of dyregulated proteostasis to neurodevelopmental disorders.Current opinion in neurobiology · 2025Review
- Heterozygous UBR5 variants result in a neurodevelopmental syndrome with developmental delay, autism, and intellectual disability.American journal of human genetics · 2025Article
- Genetic Variant Analyses Identify Novel Candidate Autism Risk Genes from a Highly Consanguineous Cohort of 104 Families from Oman.International journal of molecular sciences · 2024Article
- Increased gene dosage of RFWD2 causes autistic-like behaviors and aberrant synaptic formation and function in mice.Molecular psychiatry · 2024Article
- Crosstalk between ubiquitination and translation in neurodevelopmental disorders.Frontiers in molecular neuroscience · 2024Review
- A novel autism-associated UBLCP1 mutation impacts proteasome regulation/activity.Translational psychiatry · 2023Article
- CNTNAP2 Protein Is Degraded by the Ubiquitin-Proteasome System and the Macroautophagy-Lysosome Pathway.Molecular neurobiology · 2023Article
- Comparing synaptic proteomes across five mouse models for autism reveals converging molecular similarities including deficits in oxidative phosphorylation and Rho GTPase signaling.Frontiers in aging neuroscience · 2023Article
- Reversal of memory and autism-related phenotypes inFrontiers in cell and developmental biology · 2023Article
- Article
- Ubiquitin proteasome system in immune regulation and therapeutics.Current opinion in pharmacology · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Dynamic changes in synaptic strength rely on de novo protein synthesis and protein degradation by the ubiquitin proteasome system (UPS). Disruption of either of these cellular processes will result in significant impairments in synaptic plasticity and memory formation. Mutations in several genes encoding regulators of mRNA translation and members of the UPS have been associated with an increased risk for the development of autism spectrum disorders. It is possible that these mutations result in a similar imbalance in protein homeostasis (proteostasis) at the synapse. This review will summarize recent work investigating the role of the UPS in synaptic plasticity at glutamatergic synapses, and propose that dysfunctional proteostasis is a common consequence of several genetic mutations linked to autism spectrum disorders. Dynamic changes in synaptic strength rely on de novo protein synthesis and protein degradation by the ubiquitin proteasome system (UPS). Disruption of either of these cellular processes will result in significant impairments in synaptic plasticity and memory formation. Mutations in several genes encoding regulators of mRNA translation (i.e. FMR1) and protein degradation (i.e. UBE3A) have been associated with an increased risk for autism spectrum disorders and intellectual disability (ASD/ID). These mutations similarly disrupt protein homeostasis (proteostasis). Compensatory changes that reset the rate of proteostasis may contribute to the neurological symptoms of ASD/ID. This review summarizes recent work investigating the role of the UPS in synaptic plasticity at glutamatergic synapses, and proposes that dysfunctional proteostasis is a common consequence of several genetic mutations linked to ASD. This article is part of a mini review series: "Synaptic Function and Dysfunction in Brain Diseases".
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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.