ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Ubiquilin-1 protects cells from oxidative stress and ischemic stroke caused tissue injury in mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Disrupting FOXO4 function confers neuroprotection against oxidative stress and ischemia-reperfusion-caused neuronal injury.bioRxiv : the preprint server for biology · 2026Article
- Genetic Deletion of Cyclophilin D Results in Enhanced Hypoxia Tolerance in Mice.Cellular and molecular neurobiology · 2026Article
- Article
- Endoplasmic reticulum stress in lung cancer.Frontiers in oncology · 2025Review
- Article
- UBQLN1 links proteostasis and mitochondria function to telomere maintenance in human embryonic stem cells.Stem cell research & therapy · 2024Article
- Autophagy and UPS pathway contribute to nicotine-induced protection effect in Parkinson's disease.Experimental brain research · 2024Article
- Genome-wide association studies of ischemic stroke based on interpretable machine learning.PeerJ. Computer science · 2024Article
- Ligustroflavone exerts neuroprotective activity through suppression of NLRP1 inflammasome in ischaemic stroke mice.Experimental and therapeutic medicine · 2023Article
- Heat Shock-Induced Extracellular Vesicles Derived from Neural Stem Cells Confer Marked Neuroprotection Against Oxidative Stress and Amyloid-β-Caused Neurotoxicity.Molecular neurobiology · 2022Article
- Impact of Cardiovascular Diseases on Ischemic Stroke Outcomes.Journal of integrative neuroscience · 2022Review
- Association of the Protein-Quality-Control Protein Ubiquilin-1 With Alzheimer's Disease BothFrontiers in neuroscience · 2022Article
- miR-337-5p promotes the development of cardiac hypertrophy by targeting Ubiquilin-1 (UBQLN1).Bioengineered · 2021Article
- Sinomenine activation of Nrf2 signaling prevents inflammation and cerebral injury in a mouse model of ischemic stroke.Experimental and therapeutic medicine · 2021Article
- UBQLN1 mediates sorafenib resistance through regulating mitochondrial biogenesis and ROS homeostasis by targeting PGC1β in hepatocellular carcinoma.Signal transduction and targeted therapy · 2021Article
- Peripherally misfolded proteins exacerbate ischemic stroke-induced neuroinflammation and brain injury.Journal of neuroinflammation · 2021Article
- Role of Ubiquilins for Brown Adipocyte Proteostasis and Thermogenesis.Frontiers in endocrinology · 2021Article
- Quality control of the mitochondrial proteome.Nature reviews. Molecular cell biology · 2021Review
- Structure, Dynamics and Function of the 26S Proteasome.Sub-cellular biochemistry · 2021Review
- Overexpression of UBQLN1 reduces neuropathology in the P497S UBQLN2 mouse model of ALS/FTD.Acta neuropathologica communications · 2020Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Ubiquilin-1 (Ubqln1 or Ubqln), a ubiquitin-like protein, mediates degradation of misfolded proteins and has been implicated in a number of pathological and physiological conditions. To better understand its function in vivo, we recently generated transgenic (Tg) mice that globally overexpress mouse Ubqln in a variety of tissues and ubqln conditional knock-out mice. The Tg mice were viable and did not show any developmental or behavioral abnormalities compared with their wild-type (WT) littermates. When subjected to oxidative stress or ischemia/reperfusion, however, ubqln Tg mice but not the WT littermates showed increased tolerance to these insults. Following ischemic stroke, ubqln Tg mice recovered motor function more rapidly than did the WT mice. In contrast, KO of ubqln exacerbated neuronal damage after stroke. In addition, KO of ubqln also caused accumulation of ubiquitinated proteins. When ubqln KO mice were crossed with a ubiquitin-proteasome system function reporter mouse, the accumulation of a proteasome surrogate substrate was observed. These results suggest that Ubqln protects mice from oxidative stress and ischemic stroke-caused neuronal injury through facilitating removal of damaged proteins. Thus, enhanced removal of unwanted proteins is a potential therapeutic strategy for treating stroke-caused neuronal injury.
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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 OpenQuestion graph.