ArticleBrain research2017
Transglutaminase 2 modulation of NF-κB signaling in astrocytes is independent of its ability to mediate astrocytic viability in ischemic injury.
Article in Brain research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Transglutaminase and its role in Alzheimer's disease: focus on mitochondria, aging, defective mitophagy, synaptic degeneration, and metabolomics.GeroScience · 2026Review
- 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
- Microglial transglutaminase 2 deficiency causes impaired synaptic remodelling and cognitive deficits in mice.Cell proliferation · 2023Article
- 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
- Article
- MicroRNA‑451 relieves inflammation in cerebral ischemia‑reperfusion via the Toll‑like receptor 4/MyD88/NF‑κB signaling pathway.Molecular medicine reports · 2019Article
- Overexpression of TG2 enhances the differentiation of ectomesenchymal stem cells into neuron‑like cells and promotes functional recovery in adult rats following spinal cord injury.Molecular medicine reports · 2019Article
- 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
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Transglutaminase 2 (TG2) is a multifunctional protein that can contribute to cell death and cell survival processes in a variety of disease contexts. Within the brain, TG2 has been shown to promote cell death in ischemic injury when expressed in astrocytes (Colak and Johnson, 2012). However, the specific functions and characteristics of astrocytic TG2 that mediate this effect are largely unknown. Therefore, the goal of this study was to investigate the role of astrocytic TG2 in mediating cellular viability processes in the context of ischemic injury, with a specific focus on its contributions to intracellular signaling cascades. We show that, in response to oxygen/glucose deprivation (OGD), acute lentiviral-mediated knockdown of TG2, as well as inhibition with an irreversible TG2 inhibitor, enhances cell survival. We also show that TG2 depletion increases nuclear factor-κB (NF-κB) signaling, whereas inhibition reduces NF-κB activity. Despite its clear contribution to NF-κB signaling, however, TG2 modulation of NF-κB signaling is not likely to be a major contributor to its ability to mediate astrocytic viability in this context. Overall, the results of this study provide insight into the role of TG2 in astrocytes and suggest possible avenues for future study of the relationship between astrocytic TG2 and ischemic injury.
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Registered trials
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