ArticleRedox biology2021
The E3 ubiquitin ligase TRIM31 is involved in cerebral ischemic injury by promoting degradation of TIGAR.
Article in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 56 citations in OpenAlex.
- The ubiquitin E3 ligase TRIM59 in myeloid cell regulates complement C3 through degrading CCAAT/enhancer binding protein β to promote neuron survival after ischemic stroke.Cell & bioscience · 2026Article
- RNA-binding protein RCAN1.1L modulates ATF2 mRNA stability to promote mitochondrial fission in acute ischemic stroke.Cell death & disease · 2026Article
- Dysfunctional TRIM31 of POMC Neurons Provokes Hypothalamic Injury and Peripheral Metabolic Disorder under Long-Term Fine Particulate Matter Exposure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TRIM56 Aggravates Cerebral Ischemia-Reperfusion Injury via Inhibiting KLF4-Activated Ferroptosis Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Roles and Mechanisms of TRIM Family Proteins in Inflammation in the Brain and Beyond.International journal of molecular sciences · 2026Review
- TRIM21 Exacerbates Ischemic Brain Injury by Promoting Astrocyte-Mediated Neuroinflammation via K63-Linked Ubiquitination of MDA5.Research (Washington, D.C.) · 2026Article
- The Role of Ubiquitination and Deubiquitination in the Pathogenesis of Acute Kidney Injury: Progress in Research.Biomedicines · 2025Review
- Trim7 aggravates ischemic stroke-associated ferroptosis by promoting ubiquitin-mediated degradation of HSPA5.Cell & bioscience · 2025Article
- Loss of Trim31 Worsens Cardiac Remodeling in a Mouse Model of Heart Failure by Enhancing the Activation of the NLRP3 Inflammasome.Inflammation · 2025Article
- The protein arginine methyltransferase PRMT1 ameliorates cerebral ischemia-reperfusion injury by suppressing RIPK1-mediated necroptosis and apoptosis.Acta pharmaceutica Sinica. B · 2025Article
- Cold exposure promotes the progression of osteoarthritis through downregulating APOE in cartilage.EMBO molecular medicine · 2025Article
- The Role and Mechanisms of Ubiquitin-Proteasome System-Mediated Ferroptosis in Neurological Disorders.Neuroscience bulletin · 2025Review
- Mechanistic exploration of ubiquitination-mediated pathways in cerebral ischemic injury.Molecular biology reports · 2024Review
- E3 ubiquitin ligase TRIM31 alleviates dopaminergic neurodegeneration by promoting proteasomal degradation of VDAC1 in Parkinson's Disease model.Cell death and differentiation · 2024Article
- p53 Orchestrates Cancer Metabolism: Unveiling Strategies to Reverse the Warburg Effect.Bulletin of mathematical biology · 2024Article
- The E3 ligase TRIM7 suppresses the tumorigenesis of gastric cancer by targeting SLC7A11.Scientific reports · 2024Article
- Unraveling the Role of the NLRP3 Inflammasome in Lymphoma: Implications in Pathogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Identifying immune cell infiltration and effective diagnostic biomarkers for ischemic stroke using bioinformatics analysis.PloS one · 2024Article
- OTUD1 ameliorates cerebral ischemic injury through inhibiting inflammation by disrupting K63-linked deubiquitination of RIP2.Journal of neuroinflammation · 2023Article
- The E3 ligase TRIM31 regulates hematopoietic stem cell homeostasis and MLL-AF9 leukemia.Haematologica · 2023Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tripartite motif (TRIM) 31 has been implicated in diverse biological and pathological conditions. However, whether TRIM31 plays a role in ischemic stroke progression is not clarified. Here we demonstrated that TRIM31 was significantly downregulated in the ischemic brain and the deficiency of TRIM31 alleviated brain injury induced by middle cerebral artery occlusion by reducing reactive oxygen species production and maintaining mitochondrial homeostasis. Mechanistically, we found that TRIM31 is an E3 ubiquitin ligase for TP53-induced glycolysis and apoptosis regulator (TIGAR), which confers protection against brain ischemia by increasing the pentose phosphate pathway flux and preserving mitochondria function. TRIM31 interacted with TIGAR and promoted the polyubiquitination of TIGAR, consequently facilitated its degradation in a proteasome-dependent pathway. Furthermore, TIGAR knockdown effectively abolished the protective effect of TRIM31 deficiency after cerebral ischemia. In conclusion, we identified that TRIM31 was a novel E3 ubiquitin ligase for TIGAR, played a critical role in regulating its protein level, and subsequently involved in the ischemic brain injury, suggesting TRIM31 as a potential therapeutic target for ischemic stroke.
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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 Socratic graph.