ArticleSchizophrenia research2015
Abnormal N-acetylglucosaminyltransferase expression in prefrontal cortex in schizophrenia.
Article in Schizophrenia research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Unraveling the enigma: Post-translational modifications in psychiatric disorders and their regulatory mechanisms.Journal of translational internal medicine · 2026Article
- Molecular Modeling of the Pathogenetic Mechanisms of Neuropsychiatric Disorders.International journal of molecular sciences · 2026Review
- Metabolic Mechanisms in Electroconvulsive Therapy for Schizophrenia: Role, Potential and Future Directions.International journal of molecular sciences · 2026Review
- Review
- From Clinic to Mechanisms: Multi-Omics Provide New Insights into Cerebrospinal Fluid Metabolites and the Spectrum of Psychiatric Disorders.Molecular neurobiology · 2025Article
- Impacts of β-1, 3-N-acetylglucosaminyltransferases (B3GNTs) in human diseases.Molecular biology reports · 2024Review
- Aberrant glycosylation in schizophrenia: insights into pathophysiological mechanisms and therapeutic potentials.Frontiers in pharmacology · 2024Review
- Structural variation and eQTL analysis in two experimental populations of chickens divergently selected for feather-pecking behavior.Neurogenetics · 2023Article
- De novo mutations within metabolism networks of amino acid/protein/energy in Chinese autistic children with intellectual disability.Human genomics · 2022Article
- Review
- eQTL analysis of laying hens divergently selected for feather pecking identifies KLF14 as a potential key regulator for this behavioral disorder.Frontiers in genetics · 2022Article
- The schizophrenia susceptibility gene NAGA regulates dendritic spine density: further evidence for the dendritic spine pathology of schizophrenia.Molecular psychiatry · 2021Article
- mTOR kinase activity disrupts a phosphorylation signaling network in schizophrenia brain.Molecular psychiatry · 2021Article
- A missense variant in NDUFA6 confers schizophrenia risk by affecting YY1 binding and NAGA expression.Molecular psychiatry · 2021Article
- Galectin-3 possible involvement in antipsychotic-induced metabolic changes of schizophrenia: A minireview.World journal of diabetes · 2021Review
- Dysregulation of the unfolded protein response (UPR) in the dorsolateral prefrontal cortex in elderly patients with schizophrenia.Molecular psychiatry · 2021Article
- Aberrant glycosylation in schizophrenia: a review of 25 years of post-mortem brain studies.Molecular psychiatry · 2020Review
- Downregulated AKT-mTOR signaling pathway proteins in dorsolateral prefrontal cortex in Schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Post-translational protein modifications in schizophrenia.NPJ schizophrenia · 2020Review
- Associations between catechol-O-methyltransferase (COMT) genotypes at rs4818 and rs4680 and gene expression in human dorsolateral prefrontal cortex.Experimental brain research · 2020Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Changes in the extent of the posttranslational modification glycosylation have been previously reported in several brain regions in schizophrenia. Quality control within the endoplasmic reticulum and Golgi, branching of glycans, intracellular trafficking and targeting, protein-protein interactions, and endocytosis are processes regulated by both N-linked and O-linked glycosylation. Previous studies in schizophrenia have found altered glycan biosynthesis and abnormal glycan levels in cerebrospinal fluid (CSF) and plasma, as well as altered expression in frontal cortex of glycosyltransferase transcripts encoding proteins associated with both N- and O-linked glycosylation. The N-acetylglucosaminyltransferases (GlcNAcTs) are glycosylating enzymes that play a key role in adding N-acetylglucosamine (GlcNAc) to substrates to facilitate their proper trafficking, intracellular targeting, and cellular function. Given previous results indicating abnormal glycosylation in schizophrenia, we hypothesized that these GlcNAcTs may be abnormally expressed in this illness. We measured protein expression of nine distinct GlcNAcTs by Western blot analysis in postmortem samples of dorsolateral prefrontal cortex (DLPFC) from twelve pairs of elderly patients with schizophrenia and comparison subjects. We found decreased protein expression of UDP-GlcNAc:BetaGal Beta-1,3 GlcNAcT 8 (B3GNT8) and mannosyl (alpha-1,3-)-glycoprotein beta-1,4 GlcNAcT (MGAT4A) expression in schizophrenia. These data provide further evidence that glycosylation is dysregulated in schizophrenia, and suggest a potential mechanism associated with alterations in protein function, trafficking, and intracellular targeting in this illness.
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