Key features and details
- Sensitivity: 0.2 µg/ml
- Range: 0.117 µg/ml - 7.5 µg/ml
- Sample type: Milk, Plasma, Saliva, Serum
- Detection method: Colorimetric
- Assay type: Competitive
- Reacts with: Human
Product nameHuman Complement C3 ELISA Kit
See all C3 kits
Intra-assay Sample n Mean SD CV% Overall 5.4% Inter-assay Sample n Mean SD CV% Overall 8.3%
Sample typeSaliva, Milk, Serum, Plasma
Sensitivity= 0.2 µg/ml
Range0.117 µg/ml - 7.5 µg/ml
Assay time3h 00m
Assay durationMultiple steps standard assay
Species reactivityReacts with: Human
Human Complement C3 ELISA kit is a competitive immunoassay designed for the quantitative measurement of Complement C3 in human plasma and serum.
A Complement C3 specific antibody has been precoated onto 96-well plates and blocked. Standards or test samples are added to the wells and subsequently a Complement C3 specific biotinylated detection protein is added and then followed by washing with wash buffer. Streptavidin-Peroxidase Conjugate is added and unbound conjugates are washed away with wash buffer. TMB is then used to visualize Streptavidin-Peroxidase enzymatic reaction. TMB is catalyzed by Streptavidin-Peroxidase to produce a blue color product that changes into yellow after adding acidic stop solution. The density of yellow coloration is inversely proportional to the amount of Complement C3 captured in plate.
The entire kit may be stored at -20°C for long term storage before reconstitution - Avoid repeated freeze-thaw cycles.
Storage instructionsStore at -20°C. Please refer to protocols.
Components 1 x 96 tests 100X Streptavidin-Peroxidase Conjugate 1 x 80µl 10X Diluent M Concentrate 1 x 30ml 1X Biotinylated Human Complement C3 (Lyophilized) 1 vial 20X Wash Buffer Concentrate 1 x 30ml Chromogen Substrate 1 x 7ml Complement C3 Microplate (12 x 8 well strips) 1 unit Complement C3 Standard (Lyophilized) 1 vial Sealing Tapes 3 units Stop Solution 1 x 11ml
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
ab108822 has been referenced in 9 publications.
- Guldiken N et al. Serum transferrin as a biomarker of hepatocyte nuclear factor 4 alpha activity and hepatocyte function in liver diseases. BMC Med 19:39 (2021). PubMed: 33593348
- Brahmajothi MV & Abou-Donia MB Monitoring from Battlefield to Bedside: Serum Repositories Help Identify Biomarkers, Perspectives on Mild Traumatic Brain Injury. Mil Med 185:197-204 (2020). PubMed: 32074362
- Qu S et al. MicroRNA-194 reduces inflammatory response and human dermal microvascular endothelial cells permeability through suppression of TGF-ß/SMAD pathway by inhibiting THBS1 in chronic idiopathic urticaria. J Cell Biochem 121:111-124 (2020). PubMed: 31190349
- Lee DH et al. Identification of serum biomarkers for premature ovarian failure. Biochim Biophys Acta Proteins Proteom 1867:219-226 (2019). PubMed: 30597202
- Boire A et al. Complement Component 3 Adapts the Cerebrospinal Fluid for Leptomeningeal Metastasis. Cell 168:1101-1113.e13 (2017). PubMed: 28283064
- McGuire JL et al. The complement system, neuronal injury, and cognitive function in horizontally-acquired HIV-infected youth. J Neurovirol 22:823-830 (2016). ELISA ; Human . PubMed: 27273074
- Sweigard JH et al. Inhibition of the alternative complement pathway preserves photoreceptors after retinal injury. Sci Transl Med 7:297ra116 (2015). PubMed: 26203084
- Natrajan MS et al. Pioglitazone regulates myelin phagocytosis and multiple sclerosis monocytes. Ann Clin Transl Neurol 2:1071-84 (2015). ELISA ; Human . PubMed: 26734659
- Hepponstall M et al. Remote ischemic preconditioning (RIPC) modifies the plasma proteome in children undergoing repair of tetralogy of fallot: a randomized controlled trial. PLoS One 10:e0122778 (2015). PubMed: 25826479