Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Chimeric receptors of the human C3a receptor and C5a receptor (CD88).
Acylation-stimulating protein (ASP): structure-function determinants of cell surface binding and triacylglycerol synthetic activity.
Structure of complement receptor 2 in complex with its C3d ligand.
Mycobacterial protein HbhA binds human complement component C3.
Human anaphylatoxin (C3a) from the third component of complement. Primary structure.
Decreased infectivity despite unaltered C3 binding by a DeltahbhA mutant of Mycobacterium tuberculosis.
The chemoattractant receptor-like protein C5L2 binds the C3a des-Arg77/acylation-stimulating protein.
C5L2 is a functional receptor for acylation-stimulating protein.
Drusen complement components C3a and C5a promote choroidal neovascularization.
Human colostrum: identification of minor proteins in the aqueous phase by proteomics.
CRIg: a macrophage complement receptor required for phagocytosis of circulating pathogens.
Structure of C3b in complex with CRIg gives insights into regulation of complement activation.
Mutations in complement C3 predispose to development of atypical hemolytic uremic syndrome.
Functional basis of protection against age-related macular degeneration conferred by a common polymorphism in complement factor B.
Complement classical pathway components are all important in clearance of apoptotic and secondary necrotic cells.
Molecular basis of C-reactive protein binding and modulation of complement activation by factor H-related protein 4.
Structural basis for engagement by complement factor H of C3b on a self surface.
Protein profile of exosomes from trabecular meshwork cells.
A crystal structure of the complex between human complement receptor 2 and its ligand C3d.
Complement factor H binds malondialdehyde epitopes and protects from oxidative stress.
Proteomic analysis of microvesicles from plasma of healthy donors reveals high individual variability.
Factor H-related protein 4 activates complement by serving as a platform for the assembly of alternative pathway C3 convertase via its interaction with C3b protein.
The CD46-Jagged1 interaction is critical for human TH1 immunity.
In-depth proteomic analyses of exosomes isolated from expressed prostatic secretions in urine.
Shotgun proteomics reveals specific modulated protein patterns in tears of patients with primary open angle glaucoma naïve to therapy.
Human neutrophils secrete bioactive paucimannosidic proteins from azurophilic granules into pathogen-infected sputum.
Extracellular Fibrinogen-binding Protein (Efb) from Staphylococcus aureus Inhibits the Formation of Platelet-Leukocyte Complexes.
Mapping the Complement Factor H-Related Protein 1 (CFHR1):C3b/C3d Interactions.
CD21 and FCRL5 form a receptor complex with robust B-cell activating capacity.
A reference map of the human binary protein interactome.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Chemotactic response to human C3a and C5a anaphylatoxins. I. Evaluation of C3a and C5a leukotaxis in vitro and under stimulated in vivo conditions.
Phagocytosis of target particles bearing C3b-IgG covalent complexes by human monocytes and polymorphonuclear leucocytes.
Revealing the signaling of complement receptors C3aR and C5aR1 by anaphylatoxins.
Using brain cell-type-specific protein interactomes to interpret neurodevelopmental genetic signals in schizophrenia.
Molecular basis of anaphylatoxin binding, activation, and signaling bias at complement receptors.
IgG bearing covalently bound C3b has enhanced bactericidal activity for Escherichia coli 0111.
Granzyme K activates the entire complement cascade.
Studies in vivo and in vitro on an abnormality in the metabolism of C3 in a patient with increased susceptibility to infection.
Isolation of a fragment (C3a) of the third component of human complement containing anaphylatoxin and chemotactic activity and description of an anaphylatoxin inactivator of human serum.
Relation of putative thioester bond in C3 to activation of the alternative pathway and the binding of C3b to biological targets of complement.
Limited proteolysis of the third component of human complement, C3, by heat treatment.
gp13 (EHV-gC): a complement receptor induced by equine herpesviruses.
The role of membrane receptors for C3b and C3d in phagocytosis.
Preferential formation of C3b-IgG complexes in vitro and in vivo from nascent C3b and naturally occurring anti-band 3 antibodies.
Acylation-stimulating protein (ASP) regulates glucose transport in the rat L6 muscle cell line.
The mouse anaphylatoxin C3a receptor: molecular cloning, genomic organization, and functional expression.
Coordinated release of acylation stimulating protein (ASP) and triacylglycerol clearance by human adipose tissue in vivo in the postprandial period.
Cleavage of C3 by C3 convertases
Formation of classic pathway C5 convertase
Spontaneous hydrolysis of C3 thioester
Factor B binds to C3(H2O)
Factor D cleaves C3(H2O)-bound Factor B
Properdin stabilizes C3b:Bb bound to cell surfaces
Formation of alternative pathway C5 convertase
Factor D cleaves C3b-bound Factor B
Factor B binds to surface-associated C3b
C3(H2O):Factor Bb cleaves C3 to C3b and C3a
C3d-complexed antigen binds to complement receptor
Liganded Gi-activating GPCR acts as a GEF for Gi
C3a receptor binds anaphylatoxin C3a
Exocytosis of secretory granule lumen proteins
Exocytosis of azurophil granule lumen proteins
The Ligand:GPCR:Gi complex dissociates
Liganded Gi-activating GPCRs bind inactive heterotrimeric G-protein Gi
CPN, CPB2 cleave C3a, C5a
CR2 binds C3d, C3dg, iC3b
CR2:C3d,C3dg,iC3b binds CD19:CD81
FAM20C phosphorylates FAM20C substrates
Factor I inactivates plasma Factor H-bound C3b
Complement factor I binds to extracellular Factor H:C3b
Complement factor I binds to membrane-associated Factor H:C3b
Factor I inactivates Factor H-boundC3b
Complement factor I binds to MCP, CR1:C4b, C3b
Factor I inactivates MCP/CR1-bound C4b/C3b
CD55 (DAF) promotes C3bBb/C4bC2a dissociation
Displacement of C2a/Bb by CR1
CD55 (DAF) binds C3bBb, C4bC2a
C3b binds to cell surface
C3 convertases spontaneously dissociate
Factor H binds to membrane-associated C3b
The classical complement cascade mediates CNS synapse elimination.
Complement and microglia mediate early synapse loss in Alzheimer mouse models.
Complement receptor 3 (CD11b/CD18) is implicated in the elimination of β-amyloid peptides.
Ligand specificity of the anaphylatoxin C5L2 receptor and its regulation on myeloid and epithelial cell lines.
C5L2, a nonsignaling C5A binding protein.
Complement component C3 and complement receptor type 3 contribute to the phagocytosis and clearance of fibrillar Aβ by microglia.
Role of complement and complement membrane attack complex in laser-induced choroidal neovascularization.
Dimerization of complement factor H-related proteins modulates complement activation in vivo.