ArticleProceedings of the National Academy of Sciences of the United States of America2011
Structural basis for complement factor I control and its disease-associated sequence polymorphisms.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
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Who cites it
77 citing papers in PubMed, 137 citations in OpenAlex.
- Complement system in cancer: friend or foe of immunotherapy.Journal for immunotherapy of cancer · 2026Review
- A young woman with membranoproliferative glomerulonephritis and persistent hypocomplementemia: a case report.BMC nephrology · 2026Article
- Proteins of the SubB family provide multiple mechanisms of serum resistance inEmerging microbes & infections · 2025Article
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Complement factor I deficiency-associated neuroinflammatory disease among Old Order Amish.The Journal of allergy and clinical immunology · 2025Article
- A surface lipoprotein on Pasteurella multocida binds complement factor I to promote immune evasion.PLoS pathogens · 2025Article
- An Early Gestation Plasma Inflammasome in Rural Bangladeshi Women.Biomolecules · 2024Article
- The Lectin Pathway of the Complement System-Activation, Regulation, Disease Connections and Interplay with Other (Proteolytic) Systems.International journal of molecular sciences · 2024Review
- Functional evaluation of rare variants in complement factor I using a minigene assay.Frontiers in immunology · 2024Article
- Complement Factor I Gene Variant as a Treatable Cause of Recurrent Aseptic Neutrophilic Meningitis: A Case Report.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
- Article
- Heme Interactions as Regulators of the Alternative Pathway Complement Responses and Implications for Heme-Associated Pathologies.Current issues in molecular biology · 2023Review
- Targeted genotyping of COVID-19 patients reveals a signature of complement C3 and factor B coding SNPs associated with severe infection.Immunobiology · 2023Article
- Functional evaluation of complement factor I variants by immunoassays and SDS-PAGE.Frontiers in immunology · 2023Article
- Structural modelling of human complement FHR1 and two of its synthetic derivatives provides insight into their in-vivo functions.Computational and structural biotechnology journal · 2023Article
- Functional analysis of rare genetic variants in complement factor I in advanced age-related macular degeneration.Human molecular genetics · 2022Article
- Functional and Expressional Analyses Reveal the Distinct Role of Complement Factor I in Regulating Complement System Activation during GCRV Infection inInternational journal of molecular sciences · 2022Article
- A novel method for real-time analysis of the complement C3b:FH:FI complex reveals dominant negativeFrontiers in immunology · 2022Article
- Heme Interferes With Complement Factor I-Dependent Regulation by Enhancing Alternative Pathway Activation.Frontiers in immunology · 2022Article
- Proprotein Convertases and the Complement System.Frontiers in immunology · 2022Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The complement system is a key component of innate and adaptive immune responses. Complement regulation is critical for prevention and control of disease. We have determined the crystal structure of the complement regulatory enzyme human factor I (fI). FI is in a proteolytically inactive form, demonstrating that it circulates in a zymogen-like state despite being fully processed to the mature sequence. Mapping of functional data from mutants of fI onto the structure suggests that this inactive form is maintained by the noncatalytic heavy-chain allosterically modulating activity of the light chain. Once the ternary complex of fI, a cofactor and a substrate is formed, the allosteric inhibition is released, and fI is oriented for cleavage. In addition to explaining how circulating fI is limited to cleaving only C3b/C4b, our model explains the molecular basis of disease-associated polymorphisms in fI and its cofactors.
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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.