ELISA/assay

Monkey Complement Component 3 ELISA Kit

MBS738225

48-Strip-Wells

470 USD

ELISA Kit

Monkey Complement Component 3 ELISA Kit

Complement Component 3

complement component 3; Complement C3; complement C3; prepro-C3; C3a anaphylatoxin; complement component C3; complement component C3a; complement component C3b; acylation-stimulating protein cleavage product; epididymis secretory sperm binding protein Li 62p; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1; complement component 3; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1Cleaved into the following 11 chains:Complement C3 beta chain; Complement C3 alpha chain; C3a anaphylatoxin; Acylation stimulating protein; ASPAlternative name(s):C3adesArg

C3

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

CO3_HUMAN

Monkey

This assay has high sensitivity and excellent specificity for detection of C3. No significant cross-reactivity or interference between C3 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between C3 and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Sensitivity: 1.0 ng/mL.

Intended Uses: This C3 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Monkey C3. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Immunology

Principle of the assay: C3 ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-C3 antibody and an C3-HRP conjugate. The assay sample and buffer are incubated together with C3-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the C3 concentration since C3 from samples and C3-HRP conjugate compete for the anti-C3 antibody binding site. Since the number of sites is limited, as more sites are occupied by C3 from the sample, fewer sites are left to bind C3-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The C3 concentration in each sample is interpolated from this standard curve.

40786791

AAR89906.1

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. People with C3 deficiency are susceptible to bacterial infection. [provided by RefSeq, Feb 2009]

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: Inhibitor; Secreted; Secreted, signal peptide. Chromosomal Location of Human Ortholog: 19p13.3-p13.2. Cellular Component: extracellular space; extracellular region; plasma membrane. Molecular Function: protein binding; endopeptidase inhibitor activity; C5L2 anaphylatoxin chemotactic receptor binding; receptor binding. Biological Process: regulation of immune response; complement activation, alternative pathway; fatty acid metabolic process; signal transduction; complement activation; G-protein coupled receptor protein signaling pathway; positive regulation of angiogenesis; positive regulation of activation of membrane attack complex; positive regulation of type IIa hypersensitivity; positive regulation of G-protein coupled receptor protein signaling pathway; 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

470 USD

96-Strip-Wells

675