ReviewFrontiers in molecular neuroscience2017
E3 Ubiquitin Ligases Neurobiological Mechanisms: Development to Degeneration.
Review in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 78 citations in OpenAlex.
- Targeting of Itch by clomipramine or gene therapy improves cognitive defects related to Alzheimer's disease.iScience · 2026Article
- Recessive variants in WSB2 encoding a substrate receptor of E3 ubiquitin ligase underlie a neurodevelopmental syndrome.European journal of human genetics : EJHG · 2026Article
- Benchmarking In-Cell Proteomics for Profiling Neuroblastoma Cell Differentiation and the Ubiquitin-Proteasome System.Journal of proteome research · 2025Article
- The Ubiquitin Tale: Current Strategies and Future Challenges.ACS pharmacology & translational science · 2024Review
- A de novo ARIH2 gene mutation was detected in a patient with autism spectrum disorders and intellectual disability.Scientific reports · 2024Article
- Expression of WNT Signaling Genes in the Dorsolateral Prefrontal Cortex in Schizophrenia.Brain sciences · 2024Article
- Simulation and Computational Study of RING Domain Mutants of BRCA1 and Ube2k in AD/PD Pathophysiology.Molecular biotechnology · 2024Article
- Absence of the RING domain inLife science alliance · 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
- RNF220-mediated K63-linked polyubiquitination stabilizes Olig proteins during oligodendroglial development and myelination.Science advances · 2024Article
- Proteasome Activators and Ageing: Restoring Proteostasis Using Small Molecules.Sub-cellular biochemistry · 2024Review
- Article
- An Alzheimer's disease risk variant in TTC3 modifies the actin cytoskeleton organization and the PI3K-Akt signaling pathway in iPSC-derived forebrain neurons.Neurobiology of aging · 2023Article
- Memory phase-specific genes in the Mushroom Bodies identified using CrebB-target DamID.PLoS genetics · 2023Article
- Study of Ubiquitin Pathway Genes in a French Population with Amyotrophic Lateral Sclerosis: Focus onInternational journal of molecular sciences · 2023Article
- SANA: cross-species prediction of Gene Ontology GO annotations via topological network alignment.NPJ systems biology and applications · 2022Article
- Identification of Novel Genes for Cell Fusion during Osteoclast Formation.International journal of molecular sciences · 2022Article
- Systems-Level Analysis of Genetic Variants Reveals Functional and Spatiotemporal Context in Treatment-resistant Schizophrenia.Molecular neurobiology · 2022Article
- The Roles of NEDD4 Subfamily of HECT E3 Ubiquitin Ligases in Neurodevelopment and Neurodegeneration.International journal of molecular sciences · 2022Review
- The NEDD8-activating enzyme inhibitor MLN4924 reduces ischemic brain injury in mice.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells regularly synthesize new proteins to replace old or damaged proteins. Deposition of various aberrant proteins in specific brain regions leads to neurodegeneration and aging. The cellular protein quality control system develop various defense mechanisms against the accumulation of misfolded and aggregated proteins. The mechanisms underlying the selective recognition of specific crucial protein or misfolded proteins are majorly governed by quality control E3 ubiquitin ligases mediated through ubiquitin-proteasome system. Few known E3 ubiquitin ligases have shown prominent neurodevelopmental functions, but their interactions with different developmental proteins play critical roles in neurodevelopmental disorders. Several questions are yet to be understood properly. How E3 ubiquitin ligases determine the specificity and regulate degradation of a particular substrate involved in neuronal proliferation and differentiation is certainly the one, which needs detailed investigations. Another important question is how neurodevelopmental E3 ubiquitin ligases specifically differentiate between their versatile range of substrates and timing of their functional modulations during different phases of development. The premise of this article is to understand how few E3 ubiquitin ligases sense major molecular events, which are crucial for human brain development from its early embryonic stages to throughout adolescence period. A better understanding of these few E3 ubiquitin ligases and their interactions with other potential proteins will provide invaluable insight into disease mechanisms to approach toward therapeutic interventions.
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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.