Key features and details
- Mouse monoclonal [K13/16] to C3a / C3a des Arg
- Suitable for: IHC-P
- Reacts with: Human
- Isotype: IgG1
Product nameAnti-C3a / C3a des Arg antibody [K13/16]
See all C3a / C3a des Arg primary antibodies
DescriptionMouse monoclonal [K13/16] to C3a / C3a des Arg
SpecificityDoes not cross react with C4a or C5a.
Tested applicationsSuitable for: IHC-Pmore details
Species reactivityReacts with: Human
Full length native protein (purified) corresponding to Human C3a/ C3a des Arg.
EpitopeRecognizes an epitope present on human C3, C3a and C3a(desArg).
Effectively inhibits the biological activity of C3a in a guinea-pig platelet activation assay.
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In preparation for this, we have started to update the applications & species that this product is Abpromise guaranteed for.
We are also updating the applications & species that this product has been “predicted to work with,” however this information is not covered by our Abpromise guarantee.
Applications & species from publications and Abreviews that have not been tested in our own labs or in those of our suppliers are not covered by the Abpromise guarantee.
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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
Concentration information loading...
PurityProtein A purified
Primary antibody notesEffectively inhibits the biological activity of C3a in a guinea-pig platelet activation assay.
Light chain typekappa
sELISA pair antibody
Our Abpromise guarantee covers the use of ab36385 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
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
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human kidney tissue labelling C3a / C3a des Arg with ab36385 at a dilution of 1/150. Strong staining is visible in the of veins of nephritis.
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human liver tissue labelling C3a / C3a des Arg with ab36385 at a dilution of 1/150. Strong staining is visible in the veins.
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human tonsil tissue labelling C3a / C3a des Arg with ab36385 at a dilution of 1/150. Strong staining is visible in the lumen of veins.
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human kidney tissue labelling C3a / C3a des Arg with ab36385 at a dilution of 1/75. Strong staining is visible in the of veins of nephritis.
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
ab36385 has been referenced in 5 publications.
- Kemper C & Kolev M Enzymatic Reactions and Detection of C3 Cleavage Fragments. Bio Protoc 4:N/A (2014). PubMed: 29094056
- Elsner J et al. C3a activates reactive oxygen radical species production and intracellular calcium transients in human eosinophils. Eur J Immunol 24:518-22 (1994). PubMed: 8125125
- Elsner J et al. C3a activates the respiratory burst in human polymorphonuclear neutrophilic leukocytes via pertussis toxin-sensitive G-proteins. Blood 83:3324-31 (1994). PubMed: 8193368
- Nezlin R et al. Proteins separated from human IgG molecules. Mol Immunol 30:935-40 (1993). PubMed: 8341284
- Püschel GP et al. Increase of glucose and lactate output and decrease of flow by human anaphylatoxin C3a but not C5a in perfused rat liver. FEBS Lett 243:83-7 (1989). PubMed: 2784112