ArticleScientific reports2017
The role of the immunoproteasome in interferon-γ-mediated microglial activation.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Increased Amyloidogenic Neuronal Injury in HIV-1-infected APP-KI Alzheimer's disease mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Astrocytic LMP2 Coordinates NF-κB and TGF-β1/Smad3 Signaling to Drive Neuroinflammation after Cerebral Ischemia/Reperfusion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Postoperative neurocognitive disorder: migration and crosstalk of inflammation in the peripheral and central nervous system.Perioperative medicine (London, England) · 2026Review
- PTEN status on gonadotropin-releasing hormone (GnRH) metabolite, GnRH-(1-5), effects in endometrial cancer cell lines migration, & transcriptomic analysis of basal cell line and tumor gene expressions†.Biology of reproduction · 2025Article
- Key features of the innate immune response is mediated by the immunoproteasome in microglia.Scientific reports · 2025Article
- Targeting the immunoproteasome in hypothalamic neurons as a novel therapeutic strategy for high-fat diet-induced obesity and metabolic dysregulation.Journal of neuroinflammation · 2024Article
- Targeting Microglial Immunoproteasome: A Novel Approach in Neuroinflammatory-Related Disorders.ACS chemical neuroscience · 2024Review
- Article
- The proteasome: A key modulator of nervous system function, brain aging, and neurodegenerative disease.Frontiers in cell and developmental biology · 2023Review
- Advances in the study of the molecular biological mechanisms of radiation-induced brain injury.American journal of cancer research · 2023Review
- Article
- Addressing Blood-Brain Barrier Impairment in Alzheimer's Disease.Biomedicines · 2022Review
- Immunoproteasomes control activation of innate immune signaling and microglial function.Frontiers in immunology · 2022Article
- Article
- TDP-43 proteinopathy occurs independently of autophagic substrate accumulation and underlies nuclear defects in Niemann-Pick C disease.Neuropathology and applied neurobiology · 2021Article
- Article
- Review
- Macrocyclic Immunoproteasome Inhibitors as a Potential Therapy for Alzheimer's Disease.Journal of medicinal chemistry · 2021Article
- Survival motor neuron deficiency slows myoblast fusion through reduced myomaker and myomixer expression.Journal of cachexia, sarcopenia and muscle · 2021Article
- Omega-3 PUFAs Suppress IL-1β-Induced Hyperactivity of Immunoproteasomes in Astrocytes.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Microglia regulate the brain microenvironment by sensing damage and neutralizing potentially harmful insults. Disruption of central nervous system (CNS) homeostasis results in transition of microglia to a reactive state characterized by morphological changes and production of cytokines to prevent further damage to CNS tissue. Immunoproteasome levels are elevated in activated microglia in models of stroke, infection and traumatic brain injury, though the exact role of the immunoproteasome in neuropathology remains poorly defined. Using gene expression analysis and native gel electrophoresis we characterize the expression and assembly of the immunoproteasome in microglia following interferon-gamma exposure. Transcriptome analysis suggests that the immunoproteasome regulates multiple features of microglial activation including nitric oxide production and phagocytosis. We show that inhibiting the immunoproteasome attenuates expression of pro-inflammatory cytokines and suppresses interferon-gamma-dependent priming of microglia. These results imply that targeting immunoproteasome function following CNS injury may attenuate select microglial activity to improve the pathophysiology of neurodegenerative conditions or the progress of inflammation-mediated secondary injury following neurotrauma.
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