ArticleThe EMBO journal2017
Functional and structural insight into properdin control of complement alternative pathway amplification.
Article in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Transcriptional targets of amyotrophic lateral sclerosis/frontotemporal dementia protein TDP-43 - meta-analysis and interactive graphical database.Disease models & mechanisms · 2022Pooled it
- Three cryo-EM structures of complement C3d-bound αScience advances · 2026Article
- Shaping Tumor Microenvironment by Amplifying the Complement Cascade for Improved Immune Response in Pancreatic Cancer Model.Molecular cancer therapeutics · 2026Article
- 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
- Cryo-EM analysis of complement C3 reveals a reversible major opening of the macroglobulin ring.Nature structural & molecular biology · 2025Article
- Interactions Between the Innate and Adaptive Immune Responses.Advances in experimental medicine and biology · 2025Review
- The Complement System.Advances in experimental medicine and biology · 2025Review
- 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
- Structure determination of an unstable macromolecular complex enabled by nanobody-peptide bridging.Protein science : a publication of the Protein Society · 2022Article
- Novel homozygous CD46 variant with C-isoform expression affects C3b inactivation in atypical hemolytic uremic syndrome.European journal of immunology · 2022Article
- Structure and function of a family of tick-derived complement inhibitors targeting properdin.Nature communications · 2022Article
- Structure-Guided Engineering of a Complement Component C3-Binding Nanobody Improves Specificity and Adds Cofactor Activity.Frontiers in immunology · 2022Article
- Complement component C3: A structural perspective and potential therapeutic implications.Seminars in immunology · 2022Review
- A novel assay that characterizes properdin function shows neutrophil-derived properdin has a distinct oligomeric distribution.Frontiers in immunology · 2022Article
- Systems Biology Modeling of the Complement System Under Immune Susceptible Pathogens.Frontiers in physics · 2021Article
- Nanobodies Provide Insight into the Molecular Mechanisms of the Complement Cascade and Offer New Therapeutic Strategies.Biomolecules · 2021Review
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Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Properdin (FP) is an essential positive regulator of the complement alternative pathway (AP) providing stabilization of the C3 and C5 convertases, but its oligomeric nature challenges structural analysis. We describe here a novel FP deficiency (E244K) caused by a single point mutation which results in a very low level of AP activity. Recombinant FP E244K is monomeric, fails to support bacteriolysis, and binds weakly to C3 products. We compare this to a monomeric unit excised from oligomeric FP, which is also dysfunctional in bacteriolysis but binds the AP proconvertase, C3 convertase, C3 products and partially stabilizes the convertase. The crystal structure of such a FP-convertase complex suggests that the major contact between FP and the AP convertase is mediated by a single FP thrombospondin repeat and a small region in C3b. Small angle X-ray scattering indicates that FP E244K is trapped in a compact conformation preventing its oligomerization. Our studies demonstrate an essential role of FP oligomerization
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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.