ArticlePloS one2018
GPR108, an NF-κB activator suppressed by TIRAP, negatively regulates TLR-triggered immune responses.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- GPR108 Negatively Regulates TLR7 Signaling in Imiquimod-Induced Psoriasiform Dermatitis.Immunity, inflammation and disease · 2026Article
- Whole Exome Sequencing in 26 Saudi Patients Expands the Mutational and Clinical Spectrum of Diabetic Nephropathy.Medicina (Kaunas, Lithuania) · 2025Article
- GPR180 is a new member of the Golgi-dynamics domain seven-transmembrane helix protein family.Communications biology · 2024Article
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- Adaptor molecules mediate negative regulation of macrophage inflammatory pathways: a closer look.Frontiers in immunology · 2024Review
- Hemokinin-1 induces transcriptomic alterations in pain-related signaling processes in rat primary sensory neurons independent of NK1 tachykinin receptor activation.Frontiers in molecular neuroscience · 2023Article
- Article
- RETRACTED: Assessment of 2-Pentadecyl-2-oxazoline Role on Lipopolysaccharide-Induced Inflammation on Early Stage Development of Zebrafish (Danio rerio)Life (Basel, Switzerland) · 2022Article
- Intracellular trafficking of adeno-associated virus (AAV) vectors: challenges and future directions.Gene therapy · 2021Review
- Medical Records-Based Genetic Studies of the Complement System.Journal of the American Society of Nephrology : JASN · 2021Article
- Answered and Unanswered Questions in Early-Stage Viral Vector Transduction Biology and Innate Primary Cell Toxicity forFrontiers in immunology · 2021Review
- Pooled Screens IdentifyMolecular therapy. Methods & clinical development · 2020Article
- AAV Entry: Filling in the Blanks.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- GPR108 Is a Highly Conserved AAV Entry Factor.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Higher vertebrates have evolved innate and adaptive immune systems to defend against foreign substances and pathogens. Sophisticated regulatory circuits are needed to avoid inappropriate immune responses and inflammation. GPR108 is a seven-transmembrane family protein that activates NF-κB strongly when overexpressed. Surprisingly, its action in a physiological context is that of an antagonist of Toll-like receptor (TLR)-mediated signaling. Cells from Gpr108-null mice exhibit enhanced cytokine secretion and NF-κB and IRF3 signaling, whereas Gpr108-null macrophages reconstituted with GPR108 exhibit blunted signaling. Co-expression of TLRs and GPR108 reduces NF-κB and IFNβ promoter activation compared to expression of either TLRs or GPR108 alone. Upon TLR stimulation GPR108 abundance increases and the protein engages TLRs and their partners to reduce MyD88 expression and interfere with its binding to TLR4 through blocking MyD88 ubiquitination. In turn GPR108 is antagonized by TIRAP, an adaptor protein for TLR and MyD88. The interrelationships between GPR108 and innate immune signaling components are multifactorial and point to a membrane-associated signaling structure of significant complexity.
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