Mouse Monoclonal C3 antibody. Suitable for ELISA, IHC-P, IHC-Fr and reacts with Human samples. Cited in 1 publication.
Preservative: 0.02% Sodium azide
Constituents: PBS, 0.1% BSA
| ELISA | IHC-P | IHC-Fr | |
|---|---|---|---|
| Human | Expected | Expected | Expected |
| Species | Dilution info | Notes |
|---|---|---|
Species Human | Dilution info Use at an assay dependent concentration. | Notes - |
| Species | Dilution info | Notes |
|---|---|---|
Species Human | Dilution info Use at an assay dependent concentration. | Notes - |
| Species | Dilution info | Notes |
|---|---|---|
Species Human | Dilution info Use at an assay dependent concentration. | Notes - |
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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:10432298, PubMed:15833747, PubMed:16333141, PubMed:19615750, PubMed:2909530, PubMed:8376604, PubMed:9059512).
CPAMD1, C3, Complement C3, C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1
Mouse Monoclonal C3 antibody. Suitable for ELISA, IHC-P, IHC-Fr and reacts with Human samples. Cited in 1 publication.
Preservative: 0.02% Sodium azide
Constituents: PBS, 0.1% BSA
0.2 µm filtered antibody solution
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Complement component 3 (C3) commonly known as C3 complement is a central protein in the complement system which plays a significant role in immune response. C3b a fragment of C3 is produced when C3 undergoes cleavage. C3 is a large protein with a mass of approximately 185 kDa. The liver primarily secretes C3 into the bloodstream. It circulates in the plasma and is found in high concentration making it one of the most abundant components of the complement system.
Complement component C3 forms part of the innate immune system by promoting opsonization which enhances phagocytosis of pathogens. C3b binds to pathogens' surfaces facilitating their recognition by phagocytes. C3 as part of a complex with C3 convertase also has a role in amplifying the activation of the complement cascade. The proteolytic cleavage of C3 into C3b and C3a leads to the activation of other components forming the membrane attack complex and orchestrating inflammation.
The complement component C3 functions within both the classical and alternative complement pathways. It acts as a convergence point where the complement activation pathways meet. C3 is activated into C3b and C3a which are key to amplifying the cascade. Furthermore C3 interacts with proteins such as factor B and factor D in the alternative pathway and C4 and C2 in the classical pathway facilitating the formation of C3 convertase necessary for pathway progression.
Complement C3 shows associations with immune-related and inflammatory diseases. Deficiencies or malfunctions of complement C3 can lead to increased susceptibility to infections due to impaired opsonization and clearance of pathogens. Additionally overactivation of the complement system involving C3 can contribute to autoimmune disorders such as systemic lupus erythematosus. Other proteins linked to these diseases include C4 in lupus and factor H in age-related macular degeneration which controls complement pathway activation.
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