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Results 1 - 8 of 8
EC Number
Application
Commentary
Reference
medicine
intervention in complement-mediated pathologies by modulation of enzyme half-life through replacement of enzyme compoment C3 by the corresponding sequences of cobra venom factor from Naja kaouthia
medicine
therapeutic reduction of complement activity in vivo by use of engineered enzyme component C3 resulting in greatly improved half-life of C3 convertase
medicine
patient with membranoproliferative glomerulonephritis, preparation of naturally occuring antibodies to enzyme exhibits nephritic factor activity 60fold stronger than total IgG. Antibodies promote enzyme generation, when added to the convertase precursor or during convertase assembly
medicine
studies on role of properdin in AP complement initiation for understanding the selective predisposition of properdin-deficient patients to meningococcal infection
medicine
clinical significance of early complement stimulation in trauma patients analyzed, complement stimulation, particularly alternative pathway related to clinical outcomes in patients with severe trauma
medicine
activation of complement via the lectin pathway may be a more prominent contributor to the pathology of inflammatory reactions as compared to activation of complement via the classical pathway
medicine
Streptococcus pneumoniae induces increased gene expression of factor B of the alternative complement pathway and C3 in mouse middle ear epithelium. Activation of factor B and C3 in the middle ear lavage fluids is significantly greater than in simultaneously obtained serum samples. Complement C3 activation and opsonophagocytosis of Streptococcus pneumoniae are greatly attenuated in factor B- and factor B/C2-deficient mice. Local complement activation is an important host innate immune response and activation of the alternative complement pathway represents one of the innate immune defense mechanisms against pneumococcal infection during the early stage of acute otitis media
medicine
mutation 923DELTADG in complement factor 3 gene is identified in patients with dense deposit disease. Mutant C3923DELTADG, which lacks 2 amino acids, cannot be cleaved to C3b by the alternative pathway C3-convertase and is therefore the predominant circulating C3 protein in the patients. Upon activation to C3b by proteases, or to C3(H2O) by spontaneous thioester hydrolysis, mutant C3 generates an active C3-convertase that is regulated normally by decay accelerating factor but is resistant to decay by factor H. Activated C3b923DELTADG and C3(H2O)923DELTADG are resistant to proteolysis by factor I in the presence of factor H, but are efficiently inactivated in the presence of membrane cofactor protein, causing a fluid phase-restricted alternative pathway dysregulation in the patients that continuously activates and consumes C3 produced by the normal C3 allele
Results 1 - 8 of 8