ArticleThe Journal of biological chemistry2013
Bifunctional lipocalin ameliorates murine immune complex-induced acute lung injury.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- GPCR drug discovery: new agents, targets and indications.Nature reviews. Drug discovery · 2025Review
- Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.Frontiers in immunology · 2023Review
- Allergic eye disease: Blocking LTB4/C5 in vivo suppressed disease and Th2 & Th9 cells.Allergy · 2022Article
- Structure and function of a family of tick-derived complement inhibitors targeting properdin.Nature communications · 2022Article
- Host Immune Responses to Salivary Components - A Critical Facet of Tick-Host Interactions.Frontiers in cellular and infection microbiology · 2022Review
- Review
- Structural Characterization and Modeling of a Respiratory Syncytial Virus Fusion Glycoprotein Nanoparticle Vaccine in Solution.Molecular pharmaceutics · 2021Article
- Immunomodulatory Proteins in Tick Saliva From a Structural Perspective.Frontiers in cellular and infection microbiology · 2021Review
- A soft tick Ornithodoros moubata salivary protein OmCI is a potent inhibitor to prevent avian complement activation.Ticks and tick-borne diseases · 2020Article
- Dual inhibition of complement factor 5 and leukotriene B4 synergistically suppresses murine pemphigoid disease.JCI insight · 2019Article
- Chemical Equilibrium at the Tick-Host Feeding Interface:A Critical Examination of Biological Relevance in Hematophagous Behavior.Frontiers in physiology · 2019Review
- The rational design of affinity-attenuated OmCI for the purification of complement C5.The Journal of biological chemistry · 2018Article
- Structural basis of cholesterol binding by a novel clade of dendritic cell modulators from ticks.Scientific reports · 2017Article
- Complement factor 5 blockade reduces porcine myocardial infarction size and improves immediate cardiac function.Basic research in cardiology · 2017Article
- Structure and Ligand-Binding Mechanism of a Cysteinyl Leukotriene-Binding Protein from a Blood-Feeding Disease Vector.ACS chemical biology · 2016Article
- Structural basis for therapeutic inhibition of complement C5.Nature structural & molecular biology · 2016Article
- Combined inhibition of complement and CD14 improved outcome in porcine polymicrobial sepsis.Critical care (London, England) · 2015Article
- Are ticks venomous animals?Frontiers in zoology · 2014Article
- Complement C5 activation during influenza A infection in mice contributes to neutrophil recruitment and lung injury.PloS one · 2013Article
- Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
Molecules that simultaneously inhibit independent or co-dependent proinflammatory pathways may have advantages over conventional monotherapeutics. OmCI is a bifunctional protein derived from blood-feeding ticks that specifically prevents complement (C)-mediated C5 activation and also sequesters leukotriene B4 (LTB4) within an internal binding pocket. Here, we examined the effect of LTB4 binding on OmCI structure and function and investigated the relative importance of C-mediated C5 activation and LTB4 in a mouse model of immune complex-induced acute lung injury (IC-ALI). We describe two crystal structures of bacterially expressed OmCI: one binding a C16 fatty acid and the other binding LTB4 (C20). We show that the C5 and LTB4 binding activities of the molecule are independent of each other and that OmCI is a potent inhibitor of experimental IC-ALI, equally dependent on both C5 inhibition and LTB4 binding for full activity. The data highlight the importance of LTB4 in IC-ALI and activation of C5 by the complement pathway C5 convertase rather than by non-C proteases. The findings suggest that dual inhibition of C5 and LTB4 may be useful for treatment of human immune complex-dependent diseases.
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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.