Symbol: Name: ID: |
C3 complement component 3 GFS:2847 |
Gene name: | C3 |
Chromosome: | 19p13.3-p13.2 |
Previous Symbols: | |
Previous Names: | |
Aliases: | CPAMD1 |
Name Aliases: | |
Locus Type: | gene with protein product |
Mouse Genome Database ID: | MGI:88227 | Rat Genome Database ID: | RGD:2232 |
HGNC ID: | HGNC:1318 | RefSeq IDs: | NM_000064 |
Entrez Gene ID: | 718 | Ensembl Gene ID: | |
VEGA IDs: | OTTHUMG00000150335 | UniProt ID: | P01024 |
UCSC ID: | uc002mfm.2 | OMIM ID: | 120700 |
Pubmed: | |||
CCDS IDs: | CCDSCCDS32883.1 |
Complement component 3, often simply called C3, is a protein of the immune system. It plays a central role in the complement system and contributes to innate immunity. In humans it is encoded on chromosome 19 by a gene called C3.
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. People with C3 deficiency are susceptible to bacterial infection. [provided by RefSeq]. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Gene record to access additional publications.
Function: 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.
Function: Derived from proteolytic degradation of complement C3, C3a anaphylatoxin is a mediator of local inflammatory rocess. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release rom mast cells and basophilic leukocytes.
Products for C3 gene
Catalog | Product Name | Application | Company |
GFS:E02847 | complement component 3; ELISA kit | ELISA | n/a |
GFS:A02847 | complement component 3; Anti | ANTIBODIES | n/a |
GFS:P02847 | complement component 3; Protien | Protien | n/a |