ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2013
Dysfunction of the ubiquitin proteasome and ubiquitin-like systems in schizophrenia.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.
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Who cites it
90 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.
- A meta-analysis of ultra-high field glutamate, glutamine, GABA and glutathione 1HMRS in psychosis: Implications for studies of psychosis risk.Schizophrenia research · 2020Pooled it
- Cannabis use and glutamate across the psychosis spectrum: in vivo evidence from 7T proton magnetic resonance spectroscopy.Molecular psychiatry · 2026Article
- Unraveling the enigma: Post-translational modifications in psychiatric disorders and their regulatory mechanisms.Journal of translational internal medicine · 2026Article
- Sex Differences in Brain Cell Type-Specific Chromatin Accessibility in Schizophrenia.Biological psychiatry · 2026Article
- Cannabis Use and Glutamate across the Psychosis Spectrum: In Vivo Evidence from 7T Proton Magnetic Resonance Spectroscopy.Research square · 2025Article
- Protein aggregation identified in olfactory neuronal cells is associated with cognitive impairments in a subset of living schizophrenia patients.Molecular psychiatry · 2025Article
- Decreases in H2A monoubiquitination in the amygdala constrain fear memory formation.Learning & memory (Cold Spring Harbor, N.Y.) · 2025Article
- Ubiquitin-Proteasome-Mediated Protein Degradation and Disorders of the Central Nervous System.International journal of molecular sciences · 2025Review
- Integrating differential privacy into federated multi-task learning algorithms inBioinformatics advances · 2025Article
- UFMylation: A Potential Modification for Neurological Diseases.Current neuropharmacology · 2025Review
- Schizophrenia Biomarkers: Blood Transcriptome Suggests Two Molecular Subtypes.Neuromolecular medicine · 2024Article
- Analysis of single-cell transcriptome data from a mouse model implicates protein synthesis dysfunction in schizophrenia.Genes & genomics · 2024Article
- The ufmylation cascade controls COPII recruitment, anterograde transport, and sorting of nascent GPCRs at ER.Science advances · 2024Article
- Antipsychotic-induced epigenomic reorganization in frontal cortex of individuals with schizophrenia.eLife · 2024Article
- Sex differences in brain cell-type specific chromatin accessibility in schizophrenia.Research square · 2024Article
- Extended range proteomic analysis of blood plasma from schizophrenia patients.Frontiers in molecular biosciences · 2024Article
- Schizophrenia-associated NRXN1 deletions induce developmental-timing- and cell-type-specific vulnerabilities in human brain organoids.Nature communications · 2023Article
- Mass Spectrometry based identification of site-specific proteomic alterations and potential pathways underlying the pathophysiology of schizophrenia.Molecular biology reports · 2023Article
- Altered distribution and localization of organellar NaTranslational psychiatry · 2023Article
- UFL1, a UFMylation E3 ligase, plays a crucial role in multiple cellular stress responses.Frontiers in endocrinology · 2023Review
30 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
Abstract
Protein expression abnormalities have been implicated in the pathophysiology of schizophrenia, but the underlying cause of these changes is not known. We sought to investigate ubiquitin and ubiquitin-like (UBL) systems (SUMOylation, NEDD8ylation, and Ufmylation) as putative mechanisms underlying protein expression abnormalities seen in schizophrenia. For this, we performed western blot analysis of total ubiquitination, free ubiquitin, K48- and K63-linked ubiquitination, and E1 activases, E2 conjugases, and E3 ligases involved in ubiquitination and UBL post-translational modifications in postmortem brain tissue samples from persons with schizophrenia (n=13) and comparison subjects (n=13). We studied the superior temporal gyrus (STG) of subjects from the Mount Sinai Medical Center brain collection that were matched for age, tissue pH, and sex. We found an overall reduction of protein ubiquitination, free ubiquitin, K48-linked ubiquitination, and increased K63 polyubiquitination in schizophrenia. Ubiquitin E1 activase UBA (ubiquitin activating enzyme)-6 and E3 ligase Nedd (neural precursor cell-expressed developmentally downregulated)-4 were decreased in this illness, as were E3 ligases involved in Ufmylation (UFL1) and SUMOylation (protein inhibitor of activated STAT 3, PIAS3). NEDD8ylation was also dysregulated in schizophrenia, with decreased levels of the E1 activase UBA3 and the E3 ligase Rnf7. This study of ubiquitin and UBL systems in schizophrenia found abnormalities of ubiquitination, Ufmylation, SUMOylation, and NEDD8ylation in the STG in this disorder. These results suggest a novel approach to the understanding of schizophrenia pathophysiology, where a disruption in homeostatic adaptation of the cell underlies discreet changes seen at the protein level in this illness.
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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.