ArticleAging2020
DOK3 is involved in microglial cell activation in neuropathic pain by interacting with GPR84.
Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- GPR84 and Neuroinflammation: A Receptor Worth Targeting, or A Target Worth Reconsidering?Molecular neurobiology · 2026Review
- Illuminating proinflammatory myeloid cells with PET tracers targeting GPR84.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Magnolol Ameliorates Depression Through Modulating the TREM2-DOK3-ERK Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- GPCR drug discovery: new agents, targets and indications.Nature reviews. Drug discovery · 2025Review
- G-Protein-Coupled Receptor 84 Aggravates Early Brain Injury via Microglial NLRP3-ASC Inflammasome After Subarachnoid Hemorrhage.Brain and behavior · 2025Article
- The role of orphan G protein-coupled receptors in pain.Heliyon · 2024Review
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- Porphyromonas gingivalis Activation of Tumor-Associated Macrophages via DOK3 Promotes Recurrence of Oral Squamous Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2022Article
- Alzheimer's disease: insights from a network medicine perspective.Scientific reports · 2022Article
- Emerging roles of circular RNAs in neuropathic pain.Cell proliferation · 2021Review
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Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adaptor molecule downstream of kinase-3 (DOK3) is a vital regulator of innate immune responses in macrophages and B cells, and G-protein-coupled receptor 84 (GPR84) is significant in mediating the biosynthesis and maintenance of inflammatory mediators that are induced by neuropathic pain in microglia. In the present study, we determined the role of DOK3 in activating microglia-induced neuropathic pain and investigated the underlying mechanisms associated with GPR84. We found that knockdown of DOK3 in microglial cells dramatically reduced the levels of inflammatory factors, and we uncovered a physical association between DOK3 and GPR84 in the induction of inflammatory responses. We also observed that neuropathic pain and inflammatory responses induced by chronic constriction injury (CCI) of the sciatic nerve or intrathecal injection of a GPR84 agonist were compromised in DOK3
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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.