ELISA/assay

Complement Component 3 (C3) ELISA Kit

MBS2020086

48-Strip-Wells

550 USD

ELISA Kit

Complement Component 3 (C3) ELISA Kit

Complement Component 3 (C3)

ASP; CPAMD1; Complement Protein C3; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1; C3a anaphylatoxin; Acylation stimulating protein

Complement component 3; Complement C3; complement C3; complement component 3; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1

C3

C3; C3; ASP; C3a; C3b; AHUS5; ARMD9; CPAMD1; HEL-S-62p; CPAMD1; C3bc; ASP

CO3_HUMAN

Rat

1663

This assay has high sensitivity and excellent specificity for detection of Complement Component 3 (C3). No significant cross-reactivity or interference between Complement Component 3 (C3) and analogues was observed.

For unopened kit: All the reagents should be kept according to the labels on vials. The Standard, Detection Reagent A, Detection Reagent B and the 96-well strip plate should be stored at -20 degree C upon receipt while the others should be at 4 degree C. For opened kit: When the kit is opened, the remaining reagents still need to be stored according to the above storage condition. Besides, please return the unused wells to the foil pouch containing the desiccant pack, and reseal along entire edge of zip-seal. The stability of kit is determined by the loss rate of activity. The loss rate of this kit is less than 5% within the expiration date under appropriate storage condition. To minimize extra influence on the performance, operation procedures and lab conditions, especially room temperature, air humidity, incubator temperature should be strictly controlled. It is also strongly suggested that the whole assay is performed by the same operator from the beginning to the end.

Samples: Serum, plasma, tissue homogenates, Cell lysates, cell culture supernates and other biological fluids. Assay Type: Sandwich. Detection Range: 3.13-200ng/mL. Sensitivity: Typically less than 1.37ng/mL.

Precision: Intra-assay Precision (Precision within an assay): 3 samples with low, middle and high level Complement Component 3 (C3) were tested 20 times on one plate, respectively. Inter-assay Precision (Precision between assays): 3 samples with low, middle and high level Complement Component 3 (C3) were tested on 3 different plates, 8 replicates in each plate. CV(%) = SD/meanX100 . Intra-Assay: CV<10% . Inter-Assay: CV<12% . Assay Procedure Summary: 1. Prepare all reagents, samples and standards;. 2. Add 100uL standard or sample to each well. Incubate 2 hours at 37 degree C;. 3. Aspirate and add 100uL prepared Detection Reagent A. Incubate 1 hour at 37 degree C;. 4. Aspirate and wash 3 times;. 5. Add 100uL prepared Detection Reagent B. Incubate 30 minutes at 37 degree C;. 6. Aspirate and wash 5 times;. 7. Add 90uL Substrate Solution. Incubate 15-25 minutes at 37 degree C;. 8. Add 50uL Stop Solution. Read at 450nm immediately.

Principle of the Assay: The test principle applied in this kit is Sandwich enzyme immunoassay. The microtiter plate provided in this kit has been pre-coated with an antibody specific to Complement Component 3 (C3). Standards or samples are then added to the appropriate microtiter plate wells with a biotin-conjugated antibody specific to Complement Component 3 (C3). Next, Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. After TMB substrate solution is added, only those wells that contain Complement Component 3 (C3), biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450nm 10nm. The concentration of Complement Component 3 (C3) in the samples is then determined by comparing the O.D. of the samples to the standard curve.

152012784

AAI50180.1

P01024

187,148 Da

Activation Of C3 And C5 Pathway (106412); Adaptive Immune System Pathway (366160); Alternative Complement Activation Pathway (106410); Chagas Disease (American Trypanosomiasis) Pathway (147809); Chagas Disease (American Trypanosomiasis) Pathway (147795); Class A/1 (Rhodopsin-like Receptors) Pathway (106357); Complement Activation, Classical Pathway (198823); Complement And Coagulation Cascades Pathway (198880); Complement And Coagulation Cascades Pathway (83073); Complement And Coagulation Cascades Pathway (484)

Complement component C3 plays a central role in the activation of complement system. Its activation is required for both classical and alternative complement activation pathways. A peptide (C3a) derived from the encoded protein has antimicrobial activity, so people with C3 deficiency are susceptible to bacterial infection. [provided by RefSeq, Nov 2014]

C3: 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. Defects in C3 are the cause of complement component 3 deficiency (C3D). 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). 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). 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. 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. Increased levels of C3 and its cleavage product ASP, are associated with obesity, diabetes and coronary heart disease. Short-term endurance training reduces baseline ASP levels and subsequently fat storage. Protein type: Secreted; Inhibitor; Secreted, signal peptide. Chromosomal Location of Human Ortholog: 19p13.3-p13.2. Cellular Component: extracellular space; plasma membrane; extracellular region. Molecular Function: protein binding; endopeptidase inhibitor activity; C5L2 anaphylatoxin chemotactic receptor binding; receptor binding. Biological Process: regulation of immune response; complement activation, alternative pathway; signal transduction; fatty acid metabolic process; complement activation; G-protein coupled receptor protein signaling pathway; positive regulation of angiogenesis; positive regulation of activation of membrane attack complex; positive regulation of G-protein coupled receptor protein signaling pathway; positive regulation of type IIa hypersensitivity; regulation of complement activation; innate immune response; immune response; positive regulation of protein amino acid phosphorylation; inflammatory response; complement activation, classical pathway. Disease: Complement Component 3 Deficiency, Autosomal Recessive; Hemolytic Uremic Syndrome, Atypical, Susceptibility To, 5; Macular Degeneration, Age-related, 9

48-Strip-Wells

550 USD

96-Strip-Wells

750

5x96-Strip-Wells

2910

10x96-Strip-Wells

5220