ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Transglutaminase inhibition protects against oxidative stress-induced neuronal death downstream of pathological ERK activation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 65 citations in OpenAlex.
- Partial TG6 loss of function causes motor deficits in male mice.Human molecular genetics · 2026Article
- Transglutaminase and its role in Alzheimer's disease: focus on mitochondria, aging, defective mitophagy, synaptic degeneration, and metabolomics.GeroScience · 2026Review
- Astaxanthin effect on tissue transglutaminase expression in human neuronal differentiated stem cells exposed to hypoxia and hypoxia/reoxygenation.Scientific reports · 2026Article
- Biological Implications and Functional Significance of Transglutaminase Type 2 in Nervous System Tumors.Cells · 2024Review
- Spinocerebellar ataxia 38: structure-function analysis shows ELOVL5 G230V is proteotoxic, conformationally altered and a mutational hotspot.Human genetics · 2023Article
- Article
- Hemin-Induced Death Models Hemorrhagic Stroke and Is a Variant of Classical Neuronal Ferroptosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Exploring the Role of Transglutaminase in Patients with Glioblastoma: Current Perspectives.OncoTargets and therapy · 2022Review
- Aryl Hydrocarbon Receptor Mechanisms Affecting Chronic Kidney Disease.Frontiers in pharmacology · 2022Review
- Huntingtin-mediated axonal transport requires arginine methylation by PRMT6.Cell reports · 2021Article
- Epigenetic regulators of neuronal ferroptosis identify novel therapeutics for neurological diseases: HDACs, transglutaminases, and HIF prolyl hydroxylases.Neurobiology of disease · 2021Review
- Oxidative Stress in Parkinson's Disease: Potential Benefits of Antioxidant Supplementation.Oxidative medicine and cellular longevity · 2020Review
- High frequency electrical stimulation promotes expression of extracellular matrix proteins from human astrocytes.Molecular biology reports · 2019Article
- Gut Antibody Deficiency in a Mouse Model of CVID Results in Spontaneous Development of a Gluten-Sensitive Enteropathy.Frontiers in immunology · 2019Article
- Pharmacologic inhibition of the enzymatic effects of tissue transglutaminase reduces cardiac fibrosis and attenuates cardiomyocyte hypertrophy following pressure overload.Journal of molecular and cellular cardiology · 2018Article
- Striatal Mutant Huntingtin Protein Levels Decline with Age in Homozygous Huntington's Disease Knock-In Mouse Models.Journal of Huntington's disease · 2018Article
- Microglia Endocytose Amyloid β Through the Binding of Transglutaminase 2 and Milk Fat Globule EGF Factor 8 Protein.Neurochemical research · 2018Article
- Subcellular localization patterns of transglutaminase 2 in astrocytes and neurons are differentially altered by hypoxia.Neuroreport · 2017Article
- Amphotericin B Increases Transglutaminase 2 Expression Associated with Upregulation of Endocytotic Activity in Mouse Microglial Cell Line BV-2.Neurochemical research · 2017Article
- Indomethacin induced gene regulation in the rat hippocampus.Molecular brain · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Molecular deletion of transglutaminase 2 (TG2) has been shown to improve function and survival in a host of neurological conditions including stroke, Huntington's disease, and Parkinson's disease. However, unifying schemes by which these cross-linking or polyaminating enzymes participate broadly in neuronal death have yet to be presented. Unexpectedly, we found that in addition to TG2, TG1 gene expression level is significantly induced following stroke in vivo or due to oxidative stress in vitro. Forced expression of TG1 or TG2 proteins is sufficient to induce neuronal death in Rattus norvegicus cortical neurons in vitro. Accordingly, molecular deletion of TG2 alone is insufficient to protect Mus musculus neurons from oxidative death. By contrast, structurally diverse inhibitors used at concentrations that inhibit TG1 and TG2 simultaneously are neuroprotective. These small molecules inhibit increases in neuronal transamidating activity induced by oxidative stress; they also protect neurons downstream of pathological ERK activation when added well after the onset of the death stimulus. Together, these studies suggest that multiple TG isoforms, not only TG2, participate in oxidative stress-induced cell death signaling; and that isoform nonselective inhibitors of TG will be most efficacious in combating oxidative death in neurological disorders.
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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.