ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
CLIC1 function is required for beta-amyloid-induced generation of reactive oxygen species by microglia.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
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Who cites it
75 citing papers in PubMed, 153 citations in OpenAlex.
- CLIC1 Protein Accumulates in Circulating Monocyte Membrane during Neurodegeneration.International journal of molecular sciences · 2020Trial
- ZBTB18 Dysfunction Promotes Neuropathic Pain via CHD4-based Epigenetic Disinhibition of CLIC1 Channels in Sensory Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- A cryptic-site ligand stabilizes a non-canonical interface and blocks membrane insertion of the chloride intracellular channel CLIC1.The Journal of biological chemistry · 2026Article
- An oncostatin M receptor and chloride intracellular channel 1 crosstalk drives key oncogenic pathways in glioblastoma.Signal transduction and targeted therapy · 2026Article
- The chloride intracellular channel 1 (CLIC1) is essential for microglial morphodynamics and neuroinflammation.Science advances · 2025Article
- CLIC1 Supports Mechanisms Related to Platelet Activation and Thrombosis.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2025Article
- Circular RNA APP contributes to Alzheimer's disease pathogenesis by modulating microglial polarization via miR-1906/CLIC1 axis.Alzheimer's research & therapy · 2025Article
- Identification of an ionic mechanism for ERα-mediated rapid excitation in neurons.Science advances · 2024Article
- Retrograde AAV-mediated gene modulation reveals chloride intracellular channel proteins as potent regulators of retinal ganglion cell death.Experimental neurology · 2024Article
- Chloride ions in health and disease.Bioscience reports · 2024Review
- Chloride intracellular channel (CLIC) proteins function as fusogens.Nature communications · 2024Article
- Proteomic Analysis to Identify Prospective Biomarkers of Treatment Outcome After Microvascular Decompression for Trigeminal Neuralgia: A Preliminary Study.The journal of pain · 2024Article
- The Cl- transporter ClC-7 is essential for phagocytic clearance by microglia.Journal of cell science · 2024Article
- Microglia in Glioma.Advances in neurobiology · 2024Review
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- Protective Effects of Statins against Alzheimer Disease.Ewha medical journal · 2023Review
- Immunological characterization and diagnostic models of RNA N6-methyladenosine regulators in Alzheimer's disease.Scientific reports · 2023Article
- Human amygdala involvement in Alzheimer's disease revealed by stereological and dia-PASEF analysis.Brain pathology (Zurich, Switzerland) · 2023Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
The Alzheimer's disease (AD) brain is characterized by plaques containing beta-amyloid (Abeta) protein surrounded by astrocytes and reactive microglia. Activation of microglia by Abeta initiates production of reactive oxygen species (ROS) by the plasmalemmal NADPH oxidase; the resultant oxidative stress is thought to contribute to neurodegeneration in AD. We have previously shown that Abeta upregulates a chloride current mediated by the chloride intracellular channel 1 (CLIC1) protein in microglia. We now demonstrate that Abeta promotes the acute translocation of CLIC1 from the cytosol to the plasma membrane of microglia, where it mediates a chloride conductance. Both the Abeta induced Cl(-) conductance and ROS generation were prevented by pharmacological inhibition of CLIC1, by replacement of chloride with impermeant anions, by an anti-CLIC1 antibody and by suppression of CLIC1 expression using siRNA. Thus, the CLIC1-mediated Cl(-) conductance is required for Abeta-induced generation of neurotoxic ROS by microglia. Remarkably, CLIC1 activation is itself dependent on oxidation by ROS derived from the activated NADPH oxidase. We therefore propose that CLIC1 translocation from the cytosol to the plasma membrane, in response to redox modulation by NADPH oxidase-derived ROS, provides a feedforward mechanism that facilitates sustained microglial ROS generation by the NAPDH oxidase.
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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.