Aliases for C3 Gene
External Ids for C3 Gene
Complement component C3 plays a central role in the activation of complement system. Its activation is required for both classical and alternative complement activation pathways. A peptide (C3a) derived from the encoded protein has antimicrobial activity, so people with C3 deficiency are susceptible to bacterial infection. [provided by RefSeq, Nov 2014]
GeneCards Summary for C3 Gene
C3 (Complement Component 3) is a Protein Coding gene. Diseases associated with C3 include hemolytic uremic syndrome, atypical 5 and macular degeneration, age-related, 9. Among its related pathways are Signaling by GPCR and Class I MHC mediated antigen processing and presentation. GO annotations related to this gene include receptor binding and C5L2 anaphylatoxin chemotactic receptor binding. An important paralog of this gene is CD109.
UniProtKB/Swiss-Prot for C3 Gene
C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind covalently, via its reactive thioester, to cell surface carbohydrates or immune aggregates
Derived from proteolytic degradation of complement C3, C3a anaphylatoxin is a mediator of local inflammatory process. In chronic inflammation, acts as a chemoattractant for neutrophils (By similarity). It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.
C3-beta-c: Acts as a chemoattractant for neutrophils in chronic inflammation.
Acylation stimulating protein: adipogenic hormone that stimulates triglyceride (TG) synthesis and glucose transport in adipocytes, regulating fat storage and playing a role in postprandial TG clearance. Appears to stimulate TG synthesis via activation of the PLC, MAPK and AKT signaling pathways. Ligand for C5AR2. Promotes the phosphorylation, ARRB2-mediated internalization and recycling of C5AR2 (PubMed:8376604, PubMed:2909530, PubMed:9059512, PubMed:10432298, PubMed:15833747, PubMed:16333141, PubMed:19615750).
The complement system is a biochemical pathway involved in both innate and adaptive immune responses. There are four main functions of the complement system; lysis of microorganisms, promotion of phagocytosis, triggering inflammation and immune clearance. There are three pathways that can activate the complement system; the classical complement pathway (in response to IgG- or IgM-antigen complexes), the alternative complement pathway (spontaneous activation) and the mannose-binding lectin pathway (in response to lectin residues on pathogen cell surface membranes). All three pathway generate variants of C3 convertase, which cleaves C3 into C3a and C3b. C3a and C3b activate a series of further cleavage events that activates the complement cascade. This leads to immune defence responses such as degranulation of mast cells, increasing vascular permeability and initiation of the membrane attack pathway. Deregulation of the complement system would be extremely damaging to the host, so it is tightly regulated by complement control proteins. These regulatory proteins are found in much higher concentrations that complement proteins themselves and prevent complement system activation in self tissues. The complement system has been implicated in many autoimmune disorders, including systemic lupus erythematosus, multiple sclerosis and arthritis, and more recently has been suggested to have a pathophysiological role in Alzheimers and other neurodegenerative disorders.