Disease relevance of C3

• I(soc) was potentiated by microinjection of Clostridium C3 transferase, which inhibits Rho GTPase, whereas I(soc) was inhibited by expression of wild-type or constitutively active Rho [1].
• In the 11th patient, renal biopsy revealed an increase in mesangial matrix and cells, with deposition of IgG and C3 consistent with a mild immune-complex glomerulonephritis, and severe interstitial nephritis [2].
• Renal biopsy in all patients revealed membranoproliferative glomerulonephritis, characterized by the deposition of IgG, IgM, and C3 in glomeruli [3].
• The response to steroids suggests the efficacy of corticosteroid therapy in alleviating hemolysis due to macrophage recognition of erythrocytes coated with IgM and C3 [4].
• Histologic, electron microscopical and immunohistochemical studies revealed an early membranous glomerulonephritis characterized by the presence of subepithelial basement-membrane deposits containing IgG and C3 [5].

Psychiatry related information on C3

• The binding of C3 to NL16 is PC inhibitable, indicating that C3-16 Id is site associated [6].
• The third component of complement C3 and its fragments have a central role in a variety of host defense mechanisms [7].
• In contrast, no significant differences in neuropsychological test results were identified with respect to DNA antibody or C3 levels [8].
• Alcohol consumption and physical activity correlated inversely with C3, while no correlation was found with smoking and family history of myocardial infarction [9].
• Cerebrospinal fluid and serum immunoglobulins and C3 in Creutzfeldt-Jakob disease [10].

High impact information on C3

• CD21 binds the C3d fragment of activated C3 that becomes covalently attached to targets of complement activation, and CD19 co-stimulates signaling through the antigen receptor, membrane immunoglobulin [11].
• Covalent attachment of activated complement C3 (C3d) to antigen links innate and adaptive immunity by targeting antigen to follicular dendritic cells (FDC) and B cells via specific receptors CD21 and CD35 [12].
• There were marked reductions in proteolysis of serum C3, deposition of C3 on organisms within SIGN-R1(+) spleen macrophages, and formation of C3 ligands [13].
• A pivotal step in the complement pathway is the assembly of a C3 convertase, which digests the C3 complement component to form microbial binding C3 fragments recognized by leukocytes [13].
• Surprisingly, conditional SIGN-R1 knockout mice developed deficits in C3 catabolism when given S. pneumoniae or its capsular polysaccharide intravenously [13].

Chemical compound and disease context of C3

• The increased jejunal secretion of C4, but not C3 or factor B, paralleled the clinical activity of Crohn's disease [14].
• However, of the 21 patients with partial lipodystrophy, 17 had low serum C3, with normal C4 and C2, concentrations, accompanied in 14 by a serum C3 splitting factor indistinguishable from nephritic factor, suggesting activation of the alternative pathway [15].
• Levels of properdin, factor B and C3, C5, C6, and C9 were significantly (p less than 0.05) decreased in patients with shock in comparison with those with uncomplicated bacteremia [16].
• The 17 patients receiving heparin in whom thrombocytopenia did not develop had normal levels of platelet-associated IgG and C3 [17].
• We also report that solubilized gC-2, the genetically related glycoprotein specified by HSV-2, binds to iC3-Sepharose. mAb specific for gC-1 or gC-2 and mutant viral strains were used to identify the C3-binding glycoproteins [18].

Biological context of C3

• Introducing a second mutation in the gene encoding complement factor B, which prevents C3 turnover in vivo, obviates the phenotype of Cfh(-/-) mice [19].
• The activation of C3 to C3b is promoted by zymosan or by antibody-coated erythrocytes, demonstrating participation in both the classical and alternative complement pathways [20].
• This pathway is triggered by the hydrolysis of C3, resulting in the formation of C3 convertase [19].
• In contrast, wild-type macronuclear rDNA of the C3 strain used to obtain the mutant outreplicated B strain rDNA in B/C3 heterozygote macronuclei [21].
• Sequence differences were found between wild-type B and C3 and mutant C3 rDNAs in the replication origin region, changing an upstream repeat of a highly conserved rRNA promoter element [21].

Anatomical context of C3

• One type of clone that can be induced by MGI to form Fc and C3 receptors and differentiate to mature macrophages and granulocytes (MGI+D+) was also induced by MGI to synthesize and secrete lysozyme [22].
• Cells bearing the C3 receptor constituted a distinct minority of synovial lymphocytes in frozen-tissue sections, and were found in follicle-like accumulations [23].
• The capacity of peripheral blood monocytes to increase the osmotic fragility of C3-coated erythrocytes suggests that macrophage interaction with C3-coated erythrocytes explains the observed in vivo spherocytosis [4].
• C3 component of complement secreted by established cell lines [20].
• The kidney revealed linear staining of tubular basement membranes with antiserums specific for human IgG and C3; the membranes also showed fixation of heterologous complement [24].

Associations of C3 with other chemical compounds

• Complement protein D, a serine protease participating in the formation of the C3 convertase of the alternative complement pathway, has the lowest molecular weight (23,750) and serum concentration of all complement proteins [25].
• The steady state level of the transcripts was under androgen control in three cell lines tested which had low copy numbers of the intact C3 gene, but was not regulated in a cell line which had a very high C3 gene copy number [26].
• Characteristics of C4 photosynthesis in stems and petioles of C3 flowering plants [27].
• Moreover, upregulation of epithelial C3 production by stimulation with lipopolysaccharide enhanced bacterial internalization [28].
• We have found recently that crosslinked, but not soluble, human C3 stimulates activated, but not resting, murine B cells to thymidine uptake [29].

Gene context of C3

• CR2 binds fragments of C3 that are covalently attached to glycoconjugates [30].
• A key step in the elimination of pathogens from the body is the covalent binding of complement proteins C3 and C4 to their surfaces [31].
• Complement activation at the fetomaternal interface caused the fetal loss because breeding to C3-/- mice rescued Crry-/- mice from lethality [32].
• Furthermore, microinjection of dominant negative forms of Rac and Cdc42 or of the Rho inhibitor C3 transferase blocked serum-induced DNA synthesis [33].
• MASP-1, MAp19, and direct C3-cleaving activity are associated with smaller oligomers whereas MASP-3 is found together with MASP-2 on larger oligomers [34].

Analytical, diagnostic and therapeutic context of C3

• Surface immunoglobulins were studied with use of immunofluorescence, and the C3 receptor was detected by adherence of red cells coated with antibody and complement - both are B-cell markers [23].
• Direct immunofluorescence of skin lesions revealed immune deposits (IgM, IgE, IgA, or C3) in the blood vessels of three of five patients [35].
• Immune thrombocytopenia. Use of a Coombs antiglobulin test to detect IgG and C3 on platelets [36].
• To investigate the role of complement in Crohn's disease we measured jejunal-fluid concentrations of the complement components C4, C3, and factor B by perfusion of a closed segment of the jejunum in 22 patients with Crohn's disease thought to be limited to the terminal ileum [14].
• Significant reductions in the erythrocyte-sedimentation rate, rheumatoid factor titer, and levels of hemoglobin, IgM, and C3 occurred only with true therapy (P = 0.001, 0.01, 0.03, 0.045, and 0.005, respectively) [37].

References