ArticleFrontiers in immunology2011
Structure-function studies using deletion mutants identify domains of gC1qR/p33 as potential therapeutic targets for vascular permeability and inflammation.
Article in Frontiers in immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Role of gC1qR as a modulator of endothelial cell permeability and contributor to post-stroke inflammation and edema formation.Frontiers in cellular neuroscience · 2023Review
- An approach to p32/gC1qR/HABP1: a multifunctional protein with an essential role in cancer.Journal of cancer research and clinical oncology · 2022Review
- gC1qR Antibody Can Modulate Endothelial Cell Permeability in Angioedema.Inflammation · 2022Article
- gC1qR/C1qBP/HABP-1: Structural Analysis of the Trimeric Core Region, Interactions With a Novel Panel of Monoclonal Antibodies, and Their Influence on Binding to FXII.Frontiers in immunology · 2022Article
- Computational Insights into the Interaction between Cytoadherence Receptor gC1qR and the DBLβ12 Domain of aLife (Basel, Switzerland) · 2021Article
- SARS-CoV-2 proteins regulate inflammatory, thrombotic and diabetic responses in human arterial fibroblasts.Clinical immunology (Orlando, Fla.) · 2021Article
- Pathways for bradykinin formation and interrelationship with complement as a cause of edematous lung in COVID-19 patients.The Journal of allergy and clinical immunology · 2021Article
- Overexpression of Multifunctional Protein p32 Promotes a Malignant Phenotype in Colorectal Cancer Cells.Frontiers in oncology · 2021Article
- SARS-CoV-2 Exacerbates COVID-19 Pathology Through Activation of the Complement and Kinin Systems.Frontiers in immunology · 2021Article
- The role of complement in the tumor microenvironment.Faculty reviews · 2021Review
- Genome-Wide Association Study and Pathway Analysis for Heterophil/Lymphocyte (H/L) Ratio in Chicken.Genes · 2020Article
- gC1qR/HABP1/p32 Is a Potential New Therapeutic Target Against Mesothelioma.Frontiers in oncology · 2020Article
- SLE: Novel Postulates for Therapeutic Options.Frontiers in immunology · 2020Review
- Identification of the gC1qR sites for the HIV-1 viral envelope protein gp41 and the HCV core protein: Implications in viral-specific pathogenesis and therapy.Molecular immunology · 2016Article
- Complement Protein C1q Interacts with DC-SIGNFrontiers in immunology · 2016Article
- Structural and Functional Characterization of a Single-Chain Form of the Recognition Domain of Complement Protein C1q.Frontiers in immunology · 2016Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
The endothelial cell receptor complex for kininogen (HK) comprises gC1qR, cytokeratin 1, and urokinase-type plasminogen activator receptor and is essential for activation of the kinin system that leads to bradykinin (BK) generation. Of these, gC1qR/p33 constitutes a high affinity site for HK - the BK precursor - and is therefore critical for the assembly of the kinin-generating cascade. Previous studies have identified a putative HK site within the C-terminal domain (residues 204-218) of gC1qR recognized by mAb 74.5.2. In these studies, we used information from the crystal structure of gC1qR, to engineer several deletion (Δ) mutants and test their ability to bind and/or support BK generation. While deletion of residues 204-218 (gC1qRΔ204-218), showed significantly reduced binding to HK, BK generation was not affected when tested by a sensitive bradykinin immunoassay. In fact, all of the gC1qR deletion mutants supported BK generation with the exception of gC1qRΔ154-162 and a point mutation in which Trp 233 was substituted with Gly. Binding studies also identified the existence of two additional sites at residues 144-162 and 190-202. Moreover, binding of HK to a synthetic peptide 190-202 was inhibited by mAbs 48 and 83, but not by mAb 74.5.2. Since a single residue separates domains 190-202 and 204-218, they may be part of a highly stable HK binding pocket and therefore a potential target for drug design to prevent vascular permeability and inflammation.
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Registered trials
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