ReviewTranslational stroke research2018
Protein Modifications with Ubiquitin as Response to Cerebral Ischemia-Reperfusion Injury.
Review in Translational stroke research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
32 citing papers in PubMed, 49 citations in OpenAlex.
- DcR3 Suppresses Lipopolysaccharide-Induced Aggresome-like Structures in Macrophages via Inhibition of Reactive Oxygen Species and p38 MAPK.International journal of molecular sciences · 2026Article
- The Roles of E3 Ubiquitin Ligases in Cerebral Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025Review
- Role of autophagy in neurotoxic protein's clearance following post-ischemic stroke: where we are and what we know?Molecular brain · 2025Review
- Activation of the 20S proteasome core particle prevents cell death induced by oxygen- and glucose deprivation in cultured cortical neurons.Apoptosis : an international journal on programmed cell death · 2025Article
- Lactylation and Ischemic Stroke: Research Progress and Potential Relationship.Molecular neurobiology · 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
- Lactylation: a promising therapeutic target in ischemia-reperfusion injury management.Cell death discovery · 2025Review
- Inhibition of SCFCommunications biology · 2025Article
- Research progress of deubiquitinating enzymes in cerebral ischemia-reperfusion injury.Frontiers in aging neuroscience · 2025Review
- Article
- Astragaloside IV combined with ligustrazine ameliorates abnormal mitochondrial dynamics via Drp1 SUMO/deSUMOylation in cerebral ischemia-reperfusion injury.CNS neuroscience & therapeutics · 2024Article
- Post-ischemic ubiquitination at the postsynaptic density reversibly influences the activity of ischemia-relevant kinases.Communications biology · 2024Article
- Identifying immune cell infiltration and effective diagnostic biomarkers for ischemic stroke using bioinformatics analysis.PloS one · 2024Article
- Celastrol targeting Nedd4 reduces Nrf2-mediated oxidative stress in astrocytes after ischemic stroke.Journal of pharmaceutical analysis · 2023Article
- Stroke Proteomics: From Discovery to Diagnostic and Therapeutic Applications.Circulation research · 2022Review
- Altered lncRNAs Transcriptomic Profiles in Atherosclerosis-Induced Ischemic Stroke.Cellular and molecular neurobiology · 2022Article
- Proteasome and Neuroprotective Effect of Hyperbaric Oxygen Preconditioning in Experimental Global Cerebral Ischemia in Rats.Frontiers in neurology · 2022Article
- Interruption of endolysosomal trafficking leads to stroke brain injury.Experimental neurology · 2021Article
- LncRNA MIAT enhances cerebral ischaemia/reperfusion injury in rat model via interacting with EGLN2 and reduces its ubiquitin-mediated degradation.Journal of cellular and molecular medicine · 2021Article
- Cx32 inhibits the autophagic effect of Nur77 in SH-SY5Y cells and rat brain with ischemic stroke.Aging · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Post-translational protein modifications present an elegant and energy efficient way to dynamically reprogram cellular protein properties and functions in response to homeostatic imbalance. One such protein modification is the tagging of proteins with the small modifier ubiquitin that can have an impact on protein stability, localization, interaction dynamics, and function. Ubiquitination is vital to any eukaryotic cell under physiological conditions, but even more important under stress including oxidative, genotoxic, and heat stress, where ubiquitination levels are drastically increased. Elevated levels of ubiquitin-protein conjugates are also observed in the brain after focal and global cerebral ischemia. Post-ischemic ubiquitination is immediately induced with reperfusion and transiently detected in neurons with survival potential located in the peri-infarct area. This review aims to critically discuss current knowledge and controversies on protein ubiquitination after cerebral ischemia, with special emphasis on potential mechanisms leading to elevated ubiquitination and on target identification. Further, possible functional implications of post-ischemic ubiquitination, including a relationship to SUMOylation, a neuroprotective modification, will be highlighted. The elevation in ubiquitinated proteins following cerebral ischemia is a greatly under-explored research area, the better understanding of which may contribute to the development of novel stroke therapies.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.