Key features and details
- Mouse monoclonal  to C3a / C3a des Arg
- Suitable for: WB
- Reacts with: Human
- Isotype: IgG1
Product nameAnti-C3a / C3a des Arg antibody 
See all C3a / C3a des Arg primary antibodies
DescriptionMouse monoclonal  to C3a / C3a des Arg
Specificityab11873 reacts with a neo-epitope (des-Arg) on C3a that is formed when C3 is cleaved into C3a and C3b. ab11873 recognizes C3a and C3a des arg only. It has the most affinity with C3a des arg and least affinity with C3a. The des arg variant has an about 5x higher affinity than C3a. The antibody does not recognize C3b or full C3, as it recognizes a neo-epitope that is not available on C3.
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Human
Other Immunogen Type corresponding to Human C3a/ C3a des Arg.
Database link: P01024
- Activated human serum or purified human C3adesArg protein
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Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
Storage bufferPreservative: 0.02% Sodium azide
Constituents: PBS, 0.1% BSA
Concentration information loading...
PurityProtein G purified
Purification notes0.2 µm filtered
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab11873 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use at an assay dependent concentration.
Use at an assay dependent concentration.
FunctionC3 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. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.
Involvement in diseaseDefects in C3 are the cause of complement component 3 deficiency (C3D) [MIM:613779]. A rare defect of the complement classical pathway. Patients develop recurrent, severe, pyogenic infections because of ineffective opsonization of pathogens. Some patients may also develop autoimmune disorders, such as arthralgia and vasculitic rashes, lupus-like syndrome and membranoproliferative glomerulonephritis.
Genetic variation in C3 is associated with susceptibility to age-related macular degeneration type 9 (ARMD9) [MIM:611378]. ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane.
Defects in C3 are a cause of susceptibility to hemolytic uremic syndrome atypical type 5 (AHUS5) [MIM:612925]. An atypical form of hemolytic uremic syndrome. It is a complex genetic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, renal failure and absence of episodes of enterocolitis and diarrhea. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease. Note=Susceptibility to the development of atypical hemolytic uremic syndrome can be conferred by mutations in various components of or regulatory factors in the complement cascade system. Other genes may play a role in modifying the phenotype.
Sequence similaritiesContains 1 anaphylatoxin-like domain.
Contains 1 NTR domain.
modificationsC3b 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.
Phosphorylation sites are present in the extracelllular medium.
- Information by UniProt
- Acylation stimulating protein antibody
- Acylation stimulating protein cleavage product antibody
- ASP antibody
ab11873 has been referenced in 4 publications.
- Yuan K et al. Complement C3 overexpression activates JAK2/STAT3 pathway and correlates with gastric cancer progression. J Exp Clin Cancer Res 39:9 (2020). PubMed: 31928530
- Kolev M et al. Diapedesis-Induced Integrin Signaling via LFA-1 Facilitates Tissue Immunity by Inducing Intrinsic Complement C3 Expression in Immune Cells. Immunity 52:513-527.e8 (2020). PubMed: 32187519
- Jiménez-Reinoso A et al. Human plasma C3 is essential for the development of memory B, but not T, lymphocytes. J Allergy Clin Immunol 141:1151-1154.e14 (2018). PubMed: 29113906
- Kemper C & Kolev M Enzymatic Reactions and Detection of C3 Cleavage Fragments. Bio Protoc 4:N/A (2014). PubMed: 29094056