ArticlePloS one2012
Radiation-induced c-Jun activation depends on MEK1-ERK1/2 signaling pathway in microglial cells.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 73 citations in OpenAlex.
- Paeoniflorin Attenuates Radiation-Induced Brain Injury Associated with Modulation of Microglial Polarization and ERK/MAPK Signaling.ACS omega · 2026Article
- FRA1 (Frontiers in cell and developmental biology · 2025Article
- Interplay Between Key Molecular Signaling Pathways and Immune Players Following Brain Irradiation.Mediators of inflammation · 2025Review
- Exploring Neuroprotection against Radiation-Induced Brain Injury: A Review of Key Compounds.NeuroSci · 2024Review
- A bibliometric analysis of radiation-induced brain injury: a research of the literature from 1998 to 2023.Discover oncology · 2024Article
- Microglia in radiation-induced brain injury: Cellular and molecular mechanisms and therapeutic potential.CNS neuroscience & therapeutics · 2024Review
- Galactic Cosmic Ray Particle Exposure Does Not Increase Protein Levels of Inflammation or Oxidative Stress Markers in Rat Microglial Cells In Vitro.International journal of molecular sciences · 2024Article
- Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coli.Cellular and molecular neurobiology · 2023Article
- Resolving the role of podoplanin in the motility of papillary thyroid carcinoma-derived cells using RNA sequencing.Computational and structural biotechnology journal · 2023Article
- Article
- Pathogenic mechanisms and therapeutic promise of phytochemicals and nanocarriers based drug delivery against radiotherapy-induced neurotoxic manifestations.Drug delivery · 2022Review
- Anti-leukemic principle(s) fromCytotechnology · 2022Article
- Microglia as Therapeutic Target for Radiation-Induced Brain Injury.International journal of molecular sciences · 2022Review
- Phosphorylation of guanosine monophosphate reductase triggers a GTP-dependent switch from pro- to anti-oncogenic function of EPHA4.Cell chemical biology · 2022Article
- Expression and purification of recombinant human CCL5 and its biological characterization.The protein journal · 2022Article
- Fucoxanthin Prevents Long-Term Administration l-DOPA-Induced Neurotoxicity through the ERK/JNK-c-Jun System in 6-OHDA-Lesioned Mice and PC12 Cells.Marine drugs · 2022Article
- Research progress on mechanism and imaging of temporal lobe injury induced by radiotherapy for head and neck cancer.European radiology · 2022Review
- Melatonin signalling in Schwann cells during neuroregeneration.Frontiers in cell and developmental biology · 2022Review
- Flavonoids, the Family of Plant-Derived Antioxidants Making Inroads into Novel Therapeutic Design Against Ionizing Radiation-Induced Oxidative Stress in Parkinson's Disease.Current neuropharmacology · 2022Review
- Effects of an alpha-1d adrenoreceptor antagonist (naftopidil) on bladder dysfunction after radiotherapy in female rats.International urogynecology journal · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiation-induced normal brain injury is associated with acute and/or chronic inflammatory responses, and has been a major concern in radiotherapy. Recent studies suggest that microglial activation is a potential contributor to chronic inflammatory responses following irradiation; however, the molecular mechanism underlying the response of microglia to radiation is poorly understood. c-Jun, a component of AP-1 transcription factors, potentially regulates neural cell death and neuroinflammation. We observed a rapid increase in phosphorylation of N-terminal c-Jun (on serine 63 and 73) and MAPK kinases ERK1/2, but not JNKs, in irradiated murine microglial BV2 cells. Radiation-induced c-Jun phosphorylation is dependent on the canonical MEK-ERK signaling pathway and required for both ERK1 and ERK2 function. ERK1/2 directly interact with c-Jun in vitro and in cells; meanwhile, the JNK binding domain on c-Jun is not required for its interaction with ERK kinases. Radiation-induced reactive oxygen species (ROS) potentially contribute to c-Jun phosphorylation through activating the ERK pathway. Radiation stimulates c-Jun transcriptional activity and upregulates c-Jun-regulated proinflammatory genes, such as tumor necrosis factor-α, interleukin-1β, and cyclooxygenase-2. Pharmacologic blockade of the ERK signaling pathway interferes with c-Jun activity and inhibits radiation-stimulated expression of c-Jun target genes. Overall, our study reveals that the MEK-ERK1/2 signaling pathway, but not the JNK pathway, contributes to the c-Jun-dependent microglial inflammatory response following irradiation.
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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.