ArticleProceedings of the National Academy of Sciences of the United States of America2019
Role of UCHL1 in axonal injury and functional recovery after cerebral ischemia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Neurologic Prognostication After Cardiac Arrest Using Brain Biomarkers: A Systematic Review and Meta-analysis.JAMA neurology · 2022Pooled it
- Hypothermia for Patients Requiring Evacuation of Subdural Hematoma: A Multicenter Randomized Clinical Trial.Neurocritical care · 2022Trial
- Tightly Knotted Enzymes Inhibit Protein-Protein Aggregation.bioRxiv : the preprint server for biology · 2026Article
- Neurodegeneration Biomarkers in Epilepsy: A Critical Review of Current Findings.Life (Basel, Switzerland) · 2026Review
- Plasma Biomarkers, Brain Volume, and Cognitive Performance in Service Members and Veterans With mTBI: A LIMBIC-CENC Study.JAMA network open · 2026Article
- White matter injury after brain ischemia.Experimental neurology · 2026Review
- Blood measure of neuronal death is exponentially higher with age, especially in females, and halted in Alzheimer's disease by GM-CSF treatment.Cell reports. Medicine · 2026Article
- Vagus nerve stimulation: anti-inflammatory effects in epilepsy.Frontiers in human neuroscience · 2026Article
- Article
- 13-Docosenamide Enhances Oligodendrocyte Precursor Cell Differentiation via USP33-Mediated Deubiquitination of CNR1 in Chronic Cerebral Hypoperfusion.Neuroscience bulletin · 2025Article
- Chemoproteomic Profiling of Reactive Cysteines in Response to Oxidative Stress Induced by 6-Hydroxydopamine.Proteomics · 2025Article
- Exosomal miR-146a-3p modulates neural stem cell fate through UCHL1 downregulation in spinal cord injury: implications for neuroregeneration.Acta biochimica et biophysica Sinica · 2025Article
- UCHL3: a crucial deubiquitinase in DNA damage repair and tumor progression.Cancer cell international · 2025Review
- The deubiquitinase OTUD3 plays a neuroprotective role by reducing ferroptosis induced by cerebral ischaemia reperfusion via stabilizing PLK1 via deubiquitination.Clinical and translational medicine · 2025Article
- Modified human mesenchymal stromal/stem cells restore cortical excitability after focal ischemic stroke in rats.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Integrating machine learning for the identification of ubiquitination-associated genes in moyamoya disease.Frontiers in neurology · 2025Article
- Research progress of deubiquitinating enzymes in cerebral ischemia-reperfusion injury.Frontiers in aging neuroscience · 2025Review
- Therapeutic potential of curcumin in regenerative dentistry.Frontiers in dental medicine · 2025Article
- A closer look at the role of deubiquitinating enzymes in the Hypoxia Inducible Factor pathway.Biochemical Society transactions · 2024Review
- Abolishing UCHL1's hydrolase activity exacerbates ischemia-induced axonal injury and functional deficits in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Ubiquitin C-terminal hydrolase L1 (UCHL1) is a unique brain-specific deubiquitinating enzyme. Mutations in and aberrant function of UCHL1 have been linked to many neurological disorders. UCHL1 activity protects neurons from hypoxic injury, and binding of stroke-induced reactive lipid species to the cysteine 152 (C152) of UCHL1 unfolds the protein and disrupts its function. To investigate the role of UCHL1 and its adduction by reactive lipids in inhibiting repair and recovery of function following ischemic injury, a knock-in (KI) mouse expressing the UCHL1 C152A mutation was generated. Neurons derived from KI mice had less cell death and neurite injury after hypoxia. UCHL1 C152A KI and WT mice underwent middle cerebral artery occlusion (MCAO) or sham surgery. White matter injury was significantly decreased in KI compared with WT mice 7 d after MCAO. Histological analysis revealed decreased tissue loss at 21 d after injury in KI mice. There was also significantly improved sensorimotor recovery in postischemic KI mice. K63- and K48-linked polyubiquitinated proteins were increased in penumbra of WT mouse brains but not in KI mouse brains at 24 h post MCAO. The UCHL1 C152A mutation preserved excitatory synaptic drive to pyramidal neurons and their excitability in the periinfarct zone; axonal conduction velocity recovered by 21 d post MCAO in KI mice in corpus callosum. These results demonstrate that UCHL1 activity is an important determinant of function after ischemia and further demonstrate that the C152 site of UCHL1 plays a significant role in functional recovery after stroke.
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