C3 Recombinant Rabbit Monoclonal Antibody [JF10-30] (ET1702-99)

UNIPROT #

P01024

PROTEIN NAME

C3

SYNONYMS

Acylation stimulating protein cleavage product antibody;AHUS5 antibody;ARMD9 antibody;ASP antibody;C3 and PZP like alpha 2 macroglobulin domain containing protein 1 antibody;C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1 antibody;C3 antibody;CO3_HUMAN antibody;Complement C3 antibody;Complement C3c alpha' chain fragment 2 antibody;Complement component 3 antibody;Complement factor 3 antibody;CPAMD1 antibody;HEL S 62p antibody

TISSUE SPECIFICITY

Plasma. The acylation stimulating protein (ASP) is expressed in adipocytes and released into the plasma during both the fasting and postprandial periods.

POST-TRANSLATIONAL MODIFICATION

C3b is rapidly split in two positions by factor I and a cofactor to form iC3b (inactivated C3b) and C3f which is released. Then iC3b is slowly cleaved (possibly by factor I) to form C3c (beta chain + alpha' chain fragment 1 + alpha' chain fragment 2), C3dg and C3f. Other proteases produce other fragments such as C3d or C3g. C3a is further processed by carboxypeptidases to release the C-terminal arginine residue generating the acylation stimulating protein (ASP). Levels of ASP are increased in adipocytes in the postprandial period and by insulin and dietary chylomicrons.; (Microbial infection) C3 is cleaved by Staphylococcus aureus aureolysin; this cleavage renders C3a and C3b inactive. C3b is rapidly degraded by host factors CFH and CFI preventing its deposition on the bacterial surface while C3a is further inactivated by aureolysin.; Phosphorylated by FAM20C in the extracellular medium.

SUBCELLULAR LOCATION

Secreted.

FUNCTION

Complement C3 precursor contains complement C3 beta chain, complement C3 alpha chain, C3a anaphylatoxin, complement C3b alpha chain, complement C3c fragment, complement C3dg fragment, complement C3g fragment, complement C3d fragment and complement C3f fragment. C3a, C4a, and C5a are potent anaphylatoxins that are released during complement activation, a system of ligand-surface protein interactions specific to cells of hematopoietic lineage that aids in the elimination of pathogens. C3a and C5a secretion correlates with pathophysiological phenotypes such as asthma and bacterial meningitis. Binding of these proteins to their respective G protein-coupled receptors (C3aR, C5aR), which are present on the surface of myeloid leukocytes, induces proinflammatory events such as cellular degranulation, smooth muscle contraction, arachidonic acid metabolism, cytokine release, leukocyte activation and cellular chemotaxis. C3aR is expressed in brain and activated B-lymphocytes whereas C5aR is prevalent on the surface of hepatocyte, lung, smooth muscle, and endothelial cells. Upon activation, C3aR and C5aR are susceptible to rapid GRK-mediated phosphorylation and clathrin-coated vesicle targeting. C5aR utilizes the Ras-Raf-ERK1/2 cascade and couples to Gi/G16 proteins.