Key features and details
- Rat monoclonal [11H9] to C3
- Suitable for: ICC/IF
- Reacts with: Mouse
- Isotype: IgG2a
Product nameAnti-C3 antibody [11H9]
See all C3 primary antibodies
DescriptionRat monoclonal [11H9] to C3
SpecificityThis antibody recognizes both intact C3 and its cleaved products C3b, iC3b, C3d and C3dg. The mature protein C3 has a molecular weight of approximately 190 kDa. The complement factor C3 consists of an alpha- and a beta-chain, linked by disulfide bond. C3 convertase activates C3 by cleaving the alpha chain, releasing C3a anaphylotoxin and generating C3b (alpha chain and beta chain). C3b has a molecular weight of approximately 185 kDa. C3b is rapidly split in two positions by factor I and a cofactor to form iC3b (inactivated C3b) and C3f which is released. iC3b has a molecular weight of approximately 182 kDa. Does not cross react with C4.
Tested applicationsSuitable for: ICC/IFmore details
Species reactivityReacts with: Mouse
Does not react with: Human
C57BL/6 thymocytes saturated with rat anti-Thy-1 monoclonal antibody of IgG2b subclass (RmT1).
In response to recent customer complaints for IHC-P with paraffin embedded sections we no longer guarantee this application.
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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 ab11862 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
ab11862 has been referenced in 41 publications.
- Choi YB et al. Erythropoietin-derived peptide treatment reduced neurological deficit and neuropathological changes in a mouse model of tauopathy. Alzheimers Res Ther 13:32 (2021). PubMed: 33504364
- Lau JKY et al. Melanocortin receptor activation alleviates amyloid pathology and glial reactivity in an Alzheimer's disease transgenic mouse model. Sci Rep 11:4359 (2021). PubMed: 33623128
- Mallah K et al. Complement mediates neuroinflammation and cognitive decline at extended chronic time points after traumatic brain injury. Acta Neuropathol Commun 9:72 (2021). PubMed: 33879257
- Gaindh D et al. Prolonged Beneficial Effect of Brief Erythropoietin Peptide JM4 Therapy on Chronic Relapsing EAE. Neurotherapeutics 18:401-411 (2021). PubMed: 32959273
- Garland DL et al. Complement C5 is not critical for the formation of sub-RPE deposits in Efemp1 mutant mice. Sci Rep 11:10416 (2021). PubMed: 34001980