Key features and details
- Rabbit polyclonal to C3
- Suitable for: IHC-P, IHC-Fr
- Reacts with: Mouse
- Isotype: IgG
- Research with confidence – consistent and reproducible results with every batch
- Long-term and scalable supply – powered by recombinant technology for fast production
- Success from the first experiment – confirmed specificity through extensive validation
- Ethical standards compliant – production is animal-free
Product nameAnti-C3 antibody
See all C3 primary antibodies
DescriptionRabbit polyclonal to C3
SpecificityThis polyclonal antibody detects a band approximately 120 kDa in Western blot under reducing conditions, corresponding to the C3 alpha chain.
Tested applicationsSuitable for: IHC-P, IHC-Frmore details
Species reactivityReacts with: Mouse
Unfortunately, this information is considered to be commercially sensitive
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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
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab11887 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:120700]. 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
ab11887 has been referenced in 18 publications.
- Mulfaul K et al. Toll-like Receptor 2 Facilitates Oxidative Damage-Induced Retinal Degeneration. Cell Rep 30:2209-2224.e5 (2020). PubMed: 32075760
- Hata J et al. Complement activation by autoantigen recognition in the growth process of benign prostatic hyperplasia. Sci Rep 9:20357 (2019). PubMed: 31889151
- Pauly D et al. Cell-Type-Specific Complement Expression in the Healthy and Diseased Retina. Cell Rep 29:2835-2848.e4 (2019). PubMed: 31775049
- He J et al. Microglia Mediate Synaptic Material Clearance at the Early Stage of Rats With Retinitis Pigmentosa. Front Immunol 10:912 (2019). PubMed: 31105708
- VanRyzin JW et al. Microglial Phagocytosis of Newborn Cells Is Induced by Endocannabinoids and Sculpts Sex Differences in Juvenile Rat Social Play. Neuron 102:435-449.e6 (2019). PubMed: 30827729
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