Biomaterial Database

[Direct detection C3bBb stabilizing activity in sera from hypocomplementaemic membranoproliferative glomerulonephritis (MPGN) and complement profiles of C3NeF positive cases]. 1985

S Watanabe, and H Ohi, and M Seki, and T Fujita, and M Hatano

UI	MeSH Term	Description	Entries
D003167	Complement Activation	The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.	Activation, Complement,Activations, Complement,Complement Activations
D003169	Complement Inactivator Proteins	Serum proteins that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. The complement system is tightly regulated by inactivators that accelerate the decay of intermediates and certain cell surface receptors.	Complement Cytolysis Inhibiting Proteins,Complement Cytolysis Inhibitor Proteins,Complement Inactivating Proteins,Serum Complement Inactivators,Complement Inactivators, Serum,Inactivating Proteins, Complement,Inactivator Proteins, Complement,Inactivators, Serum Complement,Proteins, Complement Inactivating,Proteins, Complement Inactivator
D003171	Complement Pathway, Classical	Complement activation initiated by the binding of COMPLEMENT C1 to ANTIGEN-ANTIBODY COMPLEXES at the COMPLEMENT C1Q subunit. This leads to the sequential activation of COMPLEMENT C1R and COMPLEMENT C1S subunits. Activated C1s cleaves COMPLEMENT C4 and COMPLEMENT C2 forming the membrane-bound classical C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.	Classical Complement Pathway,Classical Complement Activation Pathway,Complement Activation Pathway, Classical
D003178	Complement C3 Nephritic Factor	An IgG autoantibody against the ALTERNATIVE PATHWAY C3 CONVERTASE, found in serum of patients with MESANGIOCAPILLARY GLOMERULONEPHRITIS. The binding of this autoantibody to C3bBb stabilizes the enzyme thus reduces the actions of C3b inactivators (COMPLEMENT FACTOR H; COMPLEMENT FACTOR I). This abnormally stabilized enzyme induces a continuous COMPLEMENT ACTIVATION and generation of C3b thereby promoting the assembly of MEMBRANE ATTACK COMPLEX and cytolysis.	C3 NeF,C3 NeF IgG Autoantibodies,C3 NeF IgG Autoantibody,C3NeF IgG Autoantibodies,C3NeF IgG Autoantibody,C 3 Nephritic Factor,C3 Nephritic Factor,Complement 3 Nephritic Factor,Autoantibody, C3NeF IgG,IgG Autoantibody, C3NeF
D003182	Complement C5	C5 plays a central role in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C5 is cleaved by C5 CONVERTASE into COMPLEMENT C5A and COMPLEMENT C5B. The smaller fragment C5a is an ANAPHYLATOXIN and mediator of inflammatory process. The major fragment C5b binds to the membrane initiating the spontaneous assembly of the late complement components, C5-C9, into the MEMBRANE ATTACK COMPLEX.	C5 Complement,Complement 5,Complement C5, Precursor,Complement Component 5,Precursor C5,Pro-C5,Pro-complement 5,C5, Complement,C5, Precursor,C5, Precursor Complement,Complement, C5,Component 5, Complement,Precursor Complement C5,Pro C5,Pro complement 5
D005921	Glomerulonephritis	Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.	Bright Disease,Kidney Scarring,Glomerulonephritides,Scarring, Kidney
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man

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