ArticleProceedings of the National Academy of Sciences of the United States of America2013
Structural basis for the stabilization of the complement alternative pathway C3 convertase by properdin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 83 citations in OpenAlex.
- Characterizing Properdin-Inhibited C3 Nephritic Factors in Patients with Complement-Mediated Kidney Diseases.International journal of molecular sciences · 2026Article
- Bioorthogonal tuning of nanosurface opsonisationChemical communications (Cambridge, England) · 2026Article
- The Complement System in the Setting of Critical Illness-A Narrative Review.Biomolecules · 2026Review
- Complement C3 recognition by C3 convertases.Science advances · 2026Article
- Properdin deficiency or anti-properdin treatment ameliorates disease in the C3 gain-of-function mouse model of atypical haemolytic uraemic syndrome.Frontiers in immunology · 2026Article
- Proteomic analysis of plasma proteins during fentanyl withdrawal in ovariectomized female rats with and without estradiol.Journal of neuroendocrinology · 2025Article
- The role of opsonophagocytosis in killing ofCurrent research in microbial sciences · 2025Article
- Reconstitution of the alternative pathway of the complement system enables rapid delineation of the mechanism of action of novel inhibitors.The Journal of biological chemistry · 2024Article
- Cutting edge of immune response and immunosuppressants in allogeneic and xenogeneic islet transplantation.Frontiers in immunology · 2024Review
- A Monoclonal Antibody That Provides a Model for C3 Nephritic Factors.Monoclonal antibodies in immunodiagnosis and immunotherapy · 2023Article
- Structural studies offer a framework for understanding the role of properdin in the alternative pathway and beyond.Immunological reviews · 2023Review
- Quantification of the zymogenicity and the substrate-induced activity enhancement of complement factor D.Frontiers in immunology · 2023Article
- Components of the Complement Cascade Differ in Polycystic Ovary Syndrome.International journal of molecular sciences · 2022Article
- Low molecular weight polysialic acid binds to properdin and reduces the activity of the alternative complement pathway.Scientific reports · 2022Article
- A novel assay that characterizes properdin function shows neutrophil-derived properdin has a distinct oligomeric distribution.Frontiers in immunology · 2022Article
- Mathematical Modeling of Complement Pathway Dynamics for Target Validation and Selection of Drug Modalities for Complement Therapies.Frontiers in pharmacology · 2022Article
- Targeting complement components C3 and C5 for the retina: Key concepts and lingering questions.Progress in retinal and eye research · 2021Review
- Mechanisms Driving Neutrophil-Induced T-cell Immunoparalysis in Ovarian Cancer.Cancer immunology research · 2021Observational
- The Brilliance ofPathogens (Basel, Switzerland) · 2021Review
- More than a Pore: Nonlytic Antimicrobial Functions of Complement and Bacterial Strategies for Evasion.Microbiology and molecular biology reviews : MMBR · 2021Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complement is an essential component of innate immunity. Its activation results in the assembly of unstable protease complexes, denominated C3/C5 convertases, leading to inflammation and lysis. Regulatory proteins inactivate C3/C5 convertases on host surfaces to avoid collateral tissue damage. On pathogen surfaces, properdin stabilizes C3/C5 convertases to efficiently fight infection. How properdin performs this function is, however, unclear. Using electron microscopy we show that the N- and C-terminal ends of adjacent monomers in properdin oligomers conform a curly vertex that holds together the AP convertase, interacting with both the C345C and vWA domains of C3b and Bb, respectively. Properdin also promotes a large displacement of the TED (thioester-containing domain) and CUB (complement protein subcomponents C1r/C1s, urchin embryonic growth factor and bone morphogenetic protein 1) domains of C3b, which likely impairs C3-convertase inactivation by regulatory proteins. The combined effect of molecular cross-linking and structural reorganization increases stability of the C3 convertase and facilitates recruitment of fluid-phase C3 convertase to the cell surfaces. Our model explains how properdin mediates the assembly of stabilized C3/C5-convertase clusters, which helps to localize complement amplification to pathogen surfaces.
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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.