Human Complement C3 ELISA Kit (ab108823)
Key features and details
- Sensitivity: 0.3 ng/ml
- Range: 0.625 ng/ml - 40 ng/ml
- Sample type: Cell culture supernatant, Cell Lysate, Cerebral Spinal Fluid, Milk, Saliva, Urine
- Detection method: Colorimetric
- Assay type: Sandwich (quantitative)
- Reacts with: Human
Overview
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Product name
Human Complement C3 ELISA Kit
See all C3 kits -
Detection method
Colorimetric -
Precision
Intra-assay Sample n Mean SD CV% Overall 3.5% Inter-assay Sample n Mean SD CV% Overall 10% -
Sample type
Cell culture supernatant, Saliva, Milk, Urine, Cell Lysate, Cerebral Spinal Fluid -
Assay type
Sandwich (quantitative) -
Sensitivity
= 0.3 ng/ml -
Range
0.625 ng/ml - 40 ng/ml -
Recovery
97 %
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Assay time
4h 00m -
Assay duration
Multiple steps standard assay -
Species reactivity
Reacts with: Human -
Product overview
Human Complement C3 ELISA kit is designed for the quantitative measurement of Complement C3 concentrations in Human urine, milk, saliva, cerebrospinal fluid and cell culture supernatants.
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 antibody 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 directly 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.
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Platform
Microplate
Properties
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Storage instructions
Store at -20°C. Please refer to protocols. -
Components 1 x 96 tests 100X Streptavidin-Peroxidase Conjugate 1 x 80µl 10X Diluent N Concentrate 1 x 30ml 20X Wash Buffer Concentrate 2 x 30ml 50X Biotinylated Human Complement C3 Antibody 1 x 120µl Chromogen Substrate 1 x 7ml Complement C3 Microplate (12 x 8 well strips) 1 unit Complement C3 Standard 1 vial Sealing Tapes 3 units Stop Solution 1 x 11ml -
Research areas
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Function
C3 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. -
Tissue specificity
Plasma. -
Involvement in disease
Defects 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 similarities
Contains 1 anaphylatoxin-like domain.
Contains 1 NTR domain. -
Post-translational
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. -
Cellular localization
Secreted. - Information by UniProt
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Alternative names
- Acylation stimulating protein cleavage product
- AHUS5
- ARMD9
see all -
Database links
- Entrez Gene: 718 Human
- Omim: 120700 Human
- SwissProt: P01024 Human
- Unigene: 529053 Human
Associated products
Images
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Sandwich ELISA - ab108823 Complement C3 Human ELISA kitComplement C3 measured in various samples showing quantity (microgram) per mL of tested sample
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Typical Standard CurveRepresentative Standard Curve using ab108823
References (5)
ab108823 has been referenced in 5 publications.
- Chang TT et al. Plasma proteome plus site-specific N-glycoprofiling for hepatobiliary carcinomas. J Pathol Clin Res 5:199-212 (2019). PubMed: 31136099
- Pillai A et al. Complement component 3 levels in the cerebrospinal fluid of cognitively intact elderly individuals with major depressive disorder. Biomark Neuropsychiatry 1:N/A (2019). PubMed: 31942568
- Merchant ML et al. Biomarker enhanced risk prediction for development of AKI after cardiac surgery. BMC Nephrol 19:102 (2018). PubMed: 29720115
- Saini JS et al. Nicotinamide Ameliorates Disease Phenotypes in a Human iPSC Model of Age-Related Macular Degeneration. Cell Stem Cell : (2017). PubMed: 28132833
- 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
