ArticleCommunications biology2024
KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- xCT (Slc7a11) Regulation: Lessons from Cancer Research.Neurochemical research · 2026Pooled it
- Ubiquitination-dependent regulation of ferroptosis in ischemic heart and brain.Redox biology · 2026Review
- O-GlcNAcylation of IGF2BP2 promotes angiogenesis after ischemic stroke by stabilizing PPP2CA in an m6A-dependent manner : O-GlcNAcylation of IGF2BP2 alleviates ischemic brain injury.Journal of translational medicine · 2026Article
- Targeting O-GlcNAcylation: Novel Therapeutic Strategies for Neurological Disease.Molecular neurobiology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic stroke poses a significant global health risk. Currently, recanalization of blood flow through surgery or medication is the only effective means to control ischemia-reperfusion injury. This study aims to explore the role and molecular mechanism of OGT in regulating neuronal injury and motor deficits following a stroke. The MCAO and OGD/R models were established to validate the therapeutic efficacy of OGT in mitigating neuronal injury and motor dysfunction following stroke. Molecular biological techniques were employed to assess ferroptosis levels, OGT ubiquitination, and SLC7A11 O-GlcNAcylation. OGT has a therapeutic effect on motor deficits and neuronal damage after stroke by regulating SLC7A11 O-GlcNacylation-mediated ferroptosis, while the KDM2B-mediated ubiquitination pathway is responsible for changes in OGT levels. These findings are crucial for target selection and biomarker identification in stroke treatment.
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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 Socratic graph.