ArticleNature chemical biology2023
Revealing the signaling of complement receptors C3aR and C5aR1 by anaphylatoxins.
Article in Nature chemical biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 61 citations in OpenAlex.
- Basophil Extracellular Traps in Immunity and Disease.Cancers · 2026Review
- Atypical signaling, ligand recognition and selective agonist discovery of complement receptor C5aR2.Cell research · 2026Article
- Molecular basis of diverse ligand recognition and species-specific pharmacology at the complement anaphylatoxin receptor C3aR.Nature communications · 2026Article
- Complement contributes to hyperactive behavior in the 16p11.2 hemideletion mouse model.Brain, behavior, and immunity · 2026Article
- Macrophage C3aR1 Mediates Sepsis-Induced Myocardial Injury by Triggering Neutrophil Necroptosis.Journal of cellular and molecular medicine · 2026Article
- Article
- High throughput mutational characterization of the GPCR ligand C5a using yeast display and deep sequencing.Structure (London, England : 1993) · 2026Article
- Exploring the inflammatory origins of gouty arthritis: mechanistic studies based on local lesion proteomics and validation.Frontiers in immunology · 2026Article
- Exploring the Potential Value of Inflammatory Response-Associated Genes in Chronic Rhinosinusitis with Nasal Polyps: An Integrated Bioinformatics and Experimental Validation Analysis.Journal of inflammation research · 2026Article
- The Pleiotropic Effect of Complement C5a-C5aR1 Pathway in Diseases: From Immune Regulation to Targeted Therapy.International journal of molecular sciences · 2025Review
- Review
- A novel long-acting C5a-blocking cyclic peptide prevents sepsis-induced organ dysfunction via effective blockade of the inflammatory cascade.Signal transduction and targeted therapy · 2025Article
- Disease trajectory and mortality among sepsis patients: a prospective cohort study.BMC infectious diseases · 2025Article
- A Novel Class of Complement 3a Receptor Agonists and Antagonists Derived from the TLQP-21 Peptide.Journal of medicinal chemistry · 2025Article
- Review
- Single-cell profiling identifies hair cell SLC35F1 deficiency as a signature of primate cochlear aging.Nature aging · 2025Article
- Salidroside Attenuates Epilepsy and Cognitive Dysfunction in Rats by Downregulating Complement C3-C3aR Pathway-Mediated Activation of Microglia and Astrocytes.Neurochemical research · 2025Article
- Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease.Immune network · 2025Review
- Action of the Terminal Complement Pathway on Cell Membranes.The Journal of membrane biology · 2025Review
- Structural insights into GPCR signaling activated by peptide ligands: from molecular mechanism to therapeutic application.Experimental & molecular medicine · 2025Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
The complement receptors C3aR and C5aR1, whose signaling is selectively activated by anaphylatoxins C3a and C5a, are important regulators of both innate and adaptive immune responses. Dysregulations of C3aR and C5aR1 signaling lead to multiple inflammatory disorders, including sepsis, asthma and acute respiratory distress syndrome. The mechanism underlying endogenous anaphylatoxin recognition and activation of C3aR and C5aR1 remains elusive. Here we reported the structures of C3a-bound C3aR and C5a-bound C5aR1 as well as an apo-C3aR structure. These structures, combined with mutagenesis analysis, reveal a conserved recognition pattern of anaphylatoxins to the complement receptors that is different from chemokine receptors, unique pocket topologies of C3aR and C5aR1 that mediate ligand selectivity, and a common mechanism of receptor activation. These results provide crucial insights into the molecular understanding of C3aR and C5aR1 signaling and structural templates for rational drug design for treating inflammation disorders.
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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 Socratic graph.