ArticleNeurobiology of disease2012
Complete transglutaminase 2 ablation results in reduced stroke volumes and astrocytes that exhibit increased survival in response to ischemia.
Article in Neurobiology of disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Method parameters' impact on mortality and variability in mouse stroke experiments: a meta-analysis.Scientific reports · 2016Pooled it
- Transglutaminase 2 Deletion Enhances Astrocyte-to-Neuron Metabolic Support and Attenuates Subacute Pathology Following Repetitive Mild Traumatic Brain Injury.bioRxiv : the preprint server for biology · 2026Article
- The cross-linking activity of transglutaminase 2 drives α-Synuclein pathology in synucleinopathy models.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Removal or inhibition of transglutaminase 2 decreases cellular stress, supporting tissue preservation, and recovery after SCI.Acta neuropathologica communications · 2025Article
- Article
- Pharmacological inhibition of astrocytic transglutaminase 2 facilitates the expression of a neurosupportive astrocyte reactive phenotype in association with increased histone acetylation.bioRxiv : the preprint server for biology · 2024Article
- Deletion of Transglutaminase 2 from Mouse Astrocytes Significantly Improves Their Ability to Promote Neurite Outgrowth on an Inhibitory Matrix.International journal of molecular sciences · 2023Article
- Potential intervention target of atherosclerosis: Ferroptosis (Review).Molecular medicine reports · 2022Review
- Article
- Ablation of polyamine catabolic enzymes provokes Purkinje cell damage, neuroinflammation, and severe ataxia.Journal of neuroinflammation · 2020Article
- Depletion of astrocytic transglutaminase 2 improves injury outcomes.Molecular and cellular neurosciences · 2018Article
- Transglutaminase 2: Friend or foe? The discordant role in neurons and astrocytes.Journal of neuroscience research · 2018Review
- Depletion of transglutaminase 2 in neurons alters expression of extracellular matrix and signal transduction genes and compromises cell viability.Molecular and cellular neurosciences · 2018Article
- Subcellular localization patterns of transglutaminase 2 in astrocytes and neurons are differentially altered by hypoxia.Neuroreport · 2017Article
- Transglutaminase 2 modulation of NF-κB signaling in astrocytes is independent of its ability to mediate astrocytic viability in ischemic injury.Brain research · 2017Article
- The complex role of transglutaminase 2 in glioblastoma proliferation.Neuro-oncology · 2017Article
- Inhibition or ablation of transglutaminase 2 impairs astrocyte migration.Biochemical and biophysical research communications · 2017Article
- Transglutaminase 2 has opposing roles in the regulation of cellular functions as well as cell growth and death.Cell death & disease · 2016Review
- Endostatin and transglutaminase 2 are involved in fibrosis of the aging kidney.Kidney international · 2016Article
- Indomethacin induced gene regulation in the rat hippocampus.Molecular brain · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Transglutaminase 2 (TG2) is a very multifunctional protein that is ubiquitously expressed in the body. It is a Ca(2+)-dependent transamidating enzyme, a GTPase, as well as a scaffolding protein. TG2 is the predominant form of transglutaminase expressed in the mammalian nervous system. Previously, it was shown that TG2 can affect both cell death and cell survival mechanisms depending on the cell type and the stressor. In the case of ischemic stress, TG2 was previously shown to play a protective role in the models used. For example in hTG2 transgenic mice, where TG2 is overexpressed only in neurons, middle cerebral artery ligation (MCAL) resulted in smaller infarct volumes compared to wild type mice. In this study TG2 knock out mice were used to determine how endogenous TG2 affected stroke volumes. Intriguingly, infarct volumes in TG2 knock out mice were significantly smaller compared to wild type mice. As expected, primary neurons isolated from TG2 knock out mice showed decreased viability in response to oxygen-glucose deprivation. However, primary astrocytes that were isolated from TG2 knock out mice were resistant to oxygen-glucose deprivation in situ. Both wild type and knock out neurons were protected against oxygen glucose deprivation when they were co-cultured with astrocytes from TG2 knockout mice. Therefore, the decreased stroke volumes observed in TG2 knock out mice after MCAL, can be correlated with the protective effects of TG2 knock out in astrocytes in response to oxygen glucose deprivation in situ. These findings suggest that neuron-astrocyte crosstalk plays a significant role in mediating ischemic cell death and that TG2 differentially impacts cell survival depending on cell context.
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