Key features and details
- Mouse monoclonal [7C10] to C3d
- Suitable for: IHC, ELISA, WB
- Reacts with: Human
- Isotype: IgG1
Product nameAnti-C3d antibody [7C10]
See all C3d primary antibodies
DescriptionMouse monoclonal [7C10] to C3d
This product is specific to C3d, but also C3b and iC3b, since C3d is a product from C3b.
Tested applicationsSuitable for: IHC, ELISA, WBmore details
Species reactivityReacts with: Human
Full length native protein (purified) corresponding to Human C3d.
EpitopeEpitope specificity differs from that of ab17455.
- IHC-P: Human kidney tissue.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C. Avoid freeze / thaw cycle.
Storage bufferpH: 7.40
Preservative: 0.098% Sodium azide
Constituents: PBS, 2.9% Sodium chloride
Concentration information loading...
PurityProtein A purified
Light chain typekappa
Our Abpromise guarantee covers the use of ab17453 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ELISA||1/30000. Strong reaction is seen in ELISA with a C3 coat or when used as detection antibody in sandwich ELISA in combination with a polyclonal C3 antibody. ab17453 also reacts with C3b deposited on coated antibody molecules.|
|WB||Use at an assay dependent concentration. Predicted molecular weight: 187 kDa. In Western blotting after SDS-PAGE, ab17453 reacts with C3 in both reduced and unreduced forms.|
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 cleavage product antibody
- AHUS5 antibody
- ARMD9 antibody
ab17453 has been referenced in 8 publications.
- Petrosyan A et al. A glomerulus-on-a-chip to recapitulate the human glomerular filtration barrier. Nat Commun 10:3656 (2019). PubMed: 31409793
- Pathak A et al. Factor H binding proteins protect division septa on encapsulated Streptococcus pneumoniae against complement C3b deposition and amplification. Nat Commun 9:3398 (2018). PubMed: 30139996
- Hu C et al. Complement Inhibitor CRIg/FH Ameliorates Renal Ischemia Reperfusion Injury via Activation of PI3K/AKT Signaling. J Immunol 201:3717-3730 (2018). PubMed: 30429287
- Shahini N et al. The alternative complement pathway is dysregulated in patients with chronic heart failure. Sci Rep 7:42532 (2017). PubMed: 28195242
- Harboe M et al. Properdin binding to complement activating surfaces depends on initial C3b deposition. Proc Natl Acad Sci U S A 114:E534-E539 (2017). PubMed: 28069958
- de Lima A et al. Delivery route determines the presence of immune complexes on umbilical cord erythrocytes. J Matern Fetal Neonatal Med 30:2647-2652 (2017). PubMed: 27892735
- Kemper C & Kolev M Enzymatic Reactions and Detection of C3 Cleavage Fragments. Bio Protoc 4:N/A (2014). PubMed: 29094056
- Le Friec G et al. The CD46-Jagged1 interaction is critical for human T(H)1 immunity. Nat Immunol 13:1213-21 (2012). PubMed: 23086448