ArticleCell death & disease2015
The point mutation UCH-L1 C152A protects primary neurons against cyclopentenone prostaglandin-induced cytotoxicity: implications for post-ischemic neuronal injury.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Integrating machine learning for the identification of ubiquitination-associated genes in moyamoya disease.Frontiers in neurology · 2025Article
- Scalable Thiol Reactivity Profiling Identifies Azetidinyl Oxadiazoles as Cysteine-Targeting Electrophiles.Journal of the American Chemical Society · 2024Article
- 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
- Ubiquitous regulation of cerebrovascular diseases by ubiquitin-modifying enzymes.Clinical and translational medicine · 2024Review
- Systemic treatment with ubiquitin carboxy terminal hydrolase L1 TAT protein ameliorates axonal injury and reduces functional deficits after traumatic brain injury in mice.Experimental neurology · 2024Article
- Modulation of Inflammatory Response by Electromagnetic Field Stimulation in Traumatic Brain Injury in Yucatan Swine.Journal of surgery and research · 2024Article
- Role of UCHL1 in the pathogenesis of neurodegenerative diseases and brain injury.Ageing research reviews · 2023Review
- Article
- Differential Association of 4E-BP2-Interacting Proteins Is Related to Selective Delayed Neuronal Death after Ischemia.International journal of molecular sciences · 2021Article
- Abolishing UCHL1's hydrolase activity exacerbates TBI-induced axonal injury and neuronal death in mice.Experimental neurology · 2021Article
- The Role of Ubiquitin-Proteasome Pathway and Autophagy-Lysosome Pathway in Cerebral Ischemia.Oxidative medicine and cellular longevity · 2020Review
- Role of UCHL1 in axonal injury and functional recovery after cerebral ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Novel therapies for combating chronic neuropathological sequelae of TBI.Neuropharmacology · 2019Review
- Proteomic Analysis of Hippocampus in a Mouse Model of Depression Reveals Neuroprotective Function of Ubiquitin C-terminal Hydrolase L1 (UCH-L1) via Stress-induced Cysteine Oxidative Modifications.Molecular & cellular proteomics : MCP · 2018Article
- Reactive-site-centric chemoproteomics identifies a distinct class of deubiquitinase enzymes.Nature communications · 2018Article
- S-nitrosylation of UCHL1 induces its structural instability and promotes α-synuclein aggregation.Scientific reports · 2017Article
- Life and death in the trash heap: The ubiquitin proteasome pathway and UCHL1 in brain aging, neurodegenerative disease and cerebral Ischemia.Ageing research reviews · 2017Review
- In vivo transduction of neurons with TAT-UCH-L1 protects brain against controlled cortical impact injury.PloS one · 2017Article
- Ubiquitin C-terminal hydrolase L1 (UCH-L1): structure, distribution and roles in brain function and dysfunction.The Biochemical journal · 2016Review
- Protective mechanisms of microRNA-27a against oxygen-glucose deprivation-induced injuries in hippocampal neurons.Neural regeneration research · 2016Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Cyclopentenone prostaglandins (CyPGs), such as 15-deoxy-Δ(12,14)-prostaglandin J2 (15dPGJ2), are reactive prostaglandin metabolites exerting a variety of biological effects. CyPGs are produced in ischemic brain and disrupt the ubiquitin-proteasome system (UPS). Ubiquitin-C-terminal hydrolase L1 (UCH-L1) is a brain-specific deubiquitinating enzyme that has been linked to neurodegenerative diseases. Using tandem mass spectrometry (MS) analyses, we found that the C152 site of UCH-L1 is adducted by CyPGs. Mutation of C152 to alanine (C152A) inhibited CyPG modification and conserved recombinant UCH-L1 protein hydrolase activity after 15dPGJ2 treatment. A knock-in (KI) mouse expressing the UCH-L1 C152A mutation was constructed with the bacterial artificial chromosome (BAC) technique. Brain expression and distribution of UCH-L1 in the KI mouse was similar to that of wild type (WT) as determined by western blotting. Primary cortical neurons derived from KI mice were resistant to 15dPGJ2 cytotoxicity compared with neurons from WT mice as detected by the WST-1 cell viability assay and caspase-3 and poly ADP ribose polymerase (PARP) cleavage. This protective effect was accompanied with significantly less ubiquitinated protein accumulation and aggregation as well as less UCH-L1 aggregation in C152A KI primary neurons after 15dPGJ2 treatment. Additionally, 15dPGJ2-induced axonal injury was also significantly attenuated in KI neurons as compared with WT. Taken together, these studies indicate that UCH-L1 function is important in hypoxic neuronal death, and the C152 site of UCH-L1 has a significant role in neuronal survival after hypoxic/ischemic injury.
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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 OpenQuestion graph.