ArticleProceedings of the National Academy of Sciences of the United States of America2013
Role of the ubiquitin ligase E6AP/UBE3A in controlling levels of the synaptic protein Arc.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 122 citations in OpenAlex.
- Toward a Small Molecule Therapy for Angelman Syndrome: Structure-Activity Relationship Studies of 3-Aminopyrazole Phenylacetamides as PaternalJournal of medicinal chemistry · 2026Article
- Adenosine Receptor Functionality and Desensitization Machinery in a Neuronal Cell Model of Angelman Syndrome.Journal of developmental biology · 2026Article
- Autism and Human Papillomavirus (HPV) E6: A Comprehensive Review.Iranian journal of psychiatry · 2026Review
- Dysfunction of the Autophagy System and MDM2-p53 Axis Leads to the Accumulation of Amyloidogenic Proteins in Angelman Syndrome Models.International journal of molecular sciences · 2025Article
- Prenatal Exposure to Azadiradione Leads to Developmental Disabilities.Molecular neurobiology · 2025Article
- Role of androgen receptors in sexually dimorphic phenotypes in UBE3A-dependent autism spectrum disorder.iScience · 2025Article
- Pin1 promotes human CaCell communication and signaling : CCS · 2024Article
- Sex-biasing influence of autism-associatedScience advances · 2024Article
- The role of glia in the dysregulation of neuronal spinogenesis in Ube3a-dependent ASD.Experimental neurology · 2024Article
- A Survey on the Expression of the Ubiquitin Proteasome System Components HECT- and RBR-E3 Ubiquitin Ligases and E2 Ubiquitin-Conjugating and E1 Ubiquitin-Activating Enzymes during Human Brain Development.International journal of molecular sciences · 2024Article
- Disease-associated polyalanine expansion mutations impair UBA6-dependent ubiquitination.The EMBO journal · 2024Article
- UBE3A: The Role in Autism Spectrum Disorders (ASDs) and a Potential Candidate for Biomarker Studies and Designing Therapeutic Strategies.Diseases (Basel, Switzerland) · 2023Review
- Excessive Protein Accumulation and Impaired Autophagy in the Hippocampus of Angelman Syndrome Modeled in Mice.Biological psychiatry · 2023Article
- Molecular and behavioral consequences of Ube3a gene overdosage in mice.JCI insight · 2022Article
- 'Arc'-hitecture of normal cognitive aging.Ageing research reviews · 2022Review
- An Association Study of DNA Methylation and Gene Expression in Angelman Syndrome: A Bioinformatics Approach.International journal of molecular sciences · 2022Article
- Hyperexcitable Phenotypes in Induced Pluripotent Stem Cell-Derived Neurons From Patients With 15q11-q13 Duplication Syndrome, a Genetic Form of Autism.Biological psychiatry · 2021Article
- Identification of disease-linked hyperactivating mutations in UBE3A through large-scale functional variant analysis.Nature communications · 2021Article
- Secreted retrovirus-like GAG-domain-containing protein PEG10 is regulated by UBE3A and is involved in Angelman syndrome pathophysiology.Cell reports. Medicine · 2021Article
- UBE3A reinstatement as a disease-modifying therapy for Angelman syndrome.Developmental medicine and child neurology · 2021Review
17 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inactivation of the ubiquitin ligase E6 associated protein (E6AP) encoded by the UBE3A gene has been associated with development of the Angelman syndrome. Recently, it was reported that in mice, loss of E6AP expression results in increased levels of the synaptic protein Arc and a concomitant impaired synaptic function, providing an explanation for some phenotypic features of Angelman syndrome patients. Accordingly, E6AP has been shown to negatively regulate activity-regulated cytoskeleton-associated protein (Arc) and it has been suggested that E6AP targets Arc for ubiquitination and degradation. In our study, we provide evidence that Arc is not a direct substrate for E6AP and binds only weakly to E6AP, if at all. Furthermore, we show that down-regulation of E6AP expression stimulates estradiol-induced transcription of the Arc gene. Thus, we propose that Arc protein levels are controlled by E6AP at the transcriptional rather than at the posttranslational level.
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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.