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Proprotein ConvertasesComplement C3AdipocytesComplement C3-C5 ConvertasesComplement C4Complement C4aFurinProprotein Convertase 2Complement C3aComplement ActivationComplement C5Complement C4bSubtilisinsComplement C1qComplement C3bComplement C5aProprotein Convertase 1Complement System ProteinsComplement C2Proprotein Convertase 5Complement C6Complement C3cComplement C3dComplement C9Receptors, ComplementComplement Pathway, ClassicalComplement Inactivator ProteinsComplement Pathway, AlternativeComplement C1sComplement Factor BComplement Membrane Attack ComplexComplement C2aComplement C1rComplement C7Complement Activating EnzymesComplement C8Complement C1Complement Hemolytic Activity AssayAdipocytes, White3T3-L1 CellsComplement C3-C5 Convertases, Classical PathwayReceptors, Complement 3bAntigens, CD55Complement Factor HComplement C5bComplement Factor DReceptor, Anaphylatoxin C5aComplement C3-C5 Convertases, Alternative PathwayComplement Factor IAdipose TissueComplement Inactivating AgentsSerine EndopeptidasesAspartic Acid EndopeptidasesMolecular Sequence DataProtein PrecursorsComplement C1 Inactivator ProteinsNeuroendocrine Secretory Protein 7B2Receptors, Complement 3dLipolysisAmino Acid SequenceAnaphylatoxinsComplement C3 Convertase, Alternative PathwayProtein Processing, Post-TranslationalProperdinComplement Fixation TestsCobra VenomsInsulinCarboxypeptidase HGlucose Transporter Type 4Cells, CulturedRNA, MessengerAntigens, CD59Cell LineHemolysisComplement C4b-Binding ProteinComplement C3b Inactivator ProteinsPro-Opiomelanocortinalpha 1-AntitrypsinComplement Pathway, Mannose-Binding LectinAdipogenesisRecombinant ProteinsComplement C2b3T3 CellsProtein BindingMonosaccharide Transport ProteinsAdipose Tissue, BrownBacteriolysisBase SequencePituitary HormonesMice, Inbred C57BLAntigen-Antibody ComplexKineticsGlucoseImmunoglobulin GBinding SitesSteroid 21-HydroxylaseBlotting, WesternComplement C1 Inhibitor ProteinAntigens, CD46Complement C5 Convertase, Classical Pathway
Nephritic factorAlternate complemPartial lipodystrophyAlternative complemC3NeFPathwayAdiposeHypocomplementemiaMPGNLevelsActivation
Nephritic factor5
  • [ 4 ] Patients with MPGN are more likely to have low C3 levels and the presence of C3 nephritic factor (C3NeF). (medscape.com)
  • Lipodystrophy is often associated with glomerulonephritis, low C3 serum complement levels, and the presence of a C3 nephritic factor. (medscape.com)
  • C3 nephritic factor is a serum immunoglobulin G that interacts with the C3bBb alternative pathway convertase to activate C3. (medscape.com)
  • C3 nephritic factor induces the lysis of adipocytes that secrete adipsin, a product identical to complement factor D. The distribution of the lipoatrophy is postulated to be dictated by the variable amounts of adipsin secreted by the adipocytes at different locations. (medscape.com)
  • C3 nephritic factor and SLE: report of four cases and review of the literature. (medscape.com)
Alternate complem2
  • Activation of alternate complement pathway has been demonstrated in most patients. (medscape.com)
  • Activation of an alternate complement pathway, C3 hypocomplementemia with lysis of adipocytes induced by C3NeF, has been implicated. (medscape.com)
Partial lipodystrophy1
  • Model of the adipocyte destruction in acquired partial lipodystrophy showing complement activation at the adipocyte surface resulting in adipocyte lysis. (medscape.com)
Alternative complem1
  • Adipocytes synthesize factor D, the limiting component of the alternative complement pathway, which cleaves C3-bound factor B to its active enzymatic form. (medscape.com)
C3NeF1
  • Adipocytes synthesize C3, factor B, and factor D (adipsin), which allows C3bBb to be formed locally, but which usually does not result in the activation of the terminal lytic part of the complement pathway (C5-9).The IgG antibody, C3Nef, prevents the alternative complement C3-convertase C3Bb from dissociative inactivation, resulting in adipocyte lysis. (medscape.com)
Pathway6
  • Another form of lipodystrophy that fits the classification of "acquired partial" not involving the complement pathway is associated with hematopoietic stem cell transplantation (HSCT) to treat leukemia or neuroblastoma. (medscape.com)
  • This interaction results in the formation of C4b2a, which is the classic pathway C3b convertase. (medscape.com)
  • The alternative pathway utilizes C3 and factors B and D to form the alternative pathway convertase C3b,Bb. (medscape.com)
  • Small amounts of C3b are constantly being formed in the circulation, which are inactivated by factors H and I. The binding of C3b to a foreign antigen decreases its affinity for factor H and allows for the formation of increasing amounts of the alternate pathway convertase. (medscape.com)
  • The classic and alternate pathway convertases cause C3 activation, forming C3a and C3b. (medscape.com)
  • C3b is an opsonin itself, and C3 convertase facilitates the activation of the terminal pathway and the formation of the membrane attack complex C5b-9. (medscape.com)
Adipose1
Hypocomplementemia1
  • Hypocomplementemia results from increased catabolism and decreased C3 synthesis. (medscape.com)
MPGN1
  • Clinical presentations are similar for the three types of MPGN, but they manifest somewhat different mechanisms of complement activation and predisposition to recur in kidney transplants. (medscape.com)
Levels1
  • Low C3 levels are present in approximately 75% of patients with this condition. (medscape.com)
Activation1