ArticleThe Journal of biological chemistry
Nucleolin acts as the receptor for C1QTNF4 and supports C1QTNF4-mediated innate immunity modulation.
Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
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- Identifying transcriptomic signatures that mediate the causal effect of genotype on Alzheimer's disease.Frontiers in neuroscience · 2026Article
- Unveiling the roles of CTRP family in cardiac remodeling.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Autoantibodies in systemic sclerosis: From disease bystanders to pathogenic players.Journal of translational autoimmunity · 2025Review
- Anticancer potential of lactoferrin: effects, drug synergy and molecular interactions.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Review
- A multiomic atlas identifies a treatment-resistant, bone marrow progenitor-like cell population in T cell acute lymphoblastic leukemia.Nature cancer · 2025Article
- Neuraminidase as a novel therapeutic management strategy for Alzheimer's disease: evidenced through molecular docking, molecular dynamic simulation and gene expression analysis.Frontiers in chemistry · 2025Article
- The expression and biological role of complement C1s in esophageal squamous cell carcinoma.Open life sciences · 2024Article
- CTRP4/interleukin-6 receptor signaling ameliorates autoimmune encephalomyelitis by suppressing Th17 cell differentiation.The Journal of clinical investigation · 2023Article
- CTRP family in diseases associated with inflammation and metabolism: molecular mechanisms and clinical implication.Acta pharmacologica Sinica · 2023Review
- Complement 1q/Tumor Necrosis Factor-Related Proteins (CTRPs): Structure, Receptors and Signaling.Biomedicines · 2023Review
- Enhancement of Cell Adhesion byJournal of personalized medicine · 2023Article
- Single-cell multi-omics of human clonal hematopoiesis reveals that DNMT3A R882 mutations perturb early progenitor states through selective hypomethylation.Nature genetics · 2022Article
- Tacrolimus-resistant SARS-CoV-2-specific T cell products to prevent and treat severe COVID-19 in immunosuppressed patients.Molecular therapy. Methods & clinical development · 2022Article
- CTRP4 ablation impairs associative learning and memory.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Decreased serum C1Q/TNF-related protein 4 concentrations are associated with type 2 diabetes mellitus.Therapeutic advances in endocrinology and metabolism · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The C1q and TNF related 4 (C1QTNF4) protein is a structurally unique member of the C1QTNF family, a family of secreted proteins that have structural homology with both complement C1q and the tumor necrosis factor superfamily. C1QTNF4 has been linked to the autoimmune disease systemic lupus erythematosus through genetic studies; however, its role in immunity and inflammation remains poorly defined and a cell surface receptor of C1QTNF4 has yet to be identified. Here we report identification of nucleolin as a cell surface receptor of C1QTNF4 using mass spectrometric analysis. Additionally, we present evidence that the interaction between C1QTNF4 and nucleolin is mediated by the second C1q-like domain of C1QTNF4 and the C terminus of nucleolin. We show that monocytes and B cells are target cells of C1QTNF4 and observe extensive binding to dead cells. Imaging flow cytometry experiments in monocytes show that C1QTNF4 becomes actively internalized upon cell binding. Our results suggest that nucleolin may serve as a docking molecule for C1QTNF4 and act in a context-dependent manner through coreceptors. Taken together, these findings further our understanding of C1QTNF4's function in the healthy immune system and how dysfunction may contribute to the development of systemic lupus erythematosus.
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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.