ELISA/assay

Rat Complement Component 5 ELISA Kit

MBS721993

48-Strip-Wells-(Comp

470 USD

ELISA Kit

Rat Complement Component 5 ELISA Kit

Complement Component 5

Complement component 5; Complement C5; complement C5; prepro-C5; C5a anaphylatoxin; anaphylatoxin C5a analog; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 4; complement component 5; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 4Cleaved into the following 4 chains:Complement C5 beta chain; Complement C5 alpha chain; C5a anaphylatoxin; Complement C5 alpha' chain

C5

C5; C5; C5D; C5a; C5b; ECLZB; CPAMD4; CPAMD4

CO5_HUMAN

Rat

This assay has high sensitivity and excellent specificity for detection of C5. No significant cross-reactivity or interference between C5 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between C5 and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

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

Intended Uses: This C5 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Rat C5. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Immunology

Principle of the assay: C5 ELISA kit applies the quantitative sandwich enzyme immunoassay technique. The microtiter plate has been pre-coated with a monoclonal antibody specific for C5. Standards or samples are then added to the microtiter plate wells and C5 if present, will bind to the antibody pre-coated wells. In order to quantitatively determine the amount of C5 present in the sample, a standardized preparation of horseradish peroxidase (HRP)-conjugated polyclonal antibody, specific for C5 are added to each well to "sandwich" the C5 immobilized on the plate. The microtiter plate undergoes incubation, and then the wells are thoroughly washed to remove all unbound components. Next, substrate solutions are added to each well. The enzyme (HRP) and substrate are allowed to react over a short incubation period. Only those wells that contain C5 and enzyme-conjugated antibody will exhibit a change in color. The enzyme-substrate reaction is terminated by addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The C5 concentration in each sample is interpolated from this standard curve.

109731812

AAI13739.1

188,305 Da

Activation Of C3 And C5 Pathway (106412); Class A/1 (Rhodopsin-like Receptors) Pathway (106357); Complement Activation, Classical Pathway (198823); Complement And Coagulation Cascades Pathway (83073); Complement And Coagulation Cascades Pathway (484); Complement Cascade Pathway (106405); G Alpha (i) Signalling Events Pathway (119550); GPCR Downstream Signaling Pathway (119548); GPCR Ligand Binding Pathway (161020); Herpes Simplex Infection Pathway (377873)

The protein encoded by this gene is the fifth component of complement, which plays an important role in inflammatory and cell killing processes. This protein is comprised of alpha and beta polypeptide chains that are linked by a disulfide bridge. An activation peptide, C5a, which is an anaphylatoxin that possesses potent spasmogenic and chemotactic activity, is derived from the alpha polypeptide via cleavage with a convertase. The C5b macromolecular cleavage product can form a complex with the C6 complement component, and this complex is the basis for formation of the membrane attack complex, which includes additional complement components. Mutations in this gene cause complement component 5 deficiency, a disease where patients show a propensity for severe recurrent infections. Defects in this gene have also been linked to a susceptibility to liver fibrosis and to rheumatoid arthritis. [provided by RefSeq, Jul 2008]

C5: Activation of C5 by a C5 convertase initiates the spontaneous assembly of the late complement components, C5-C9, into the membrane attack complex. C5b has a transient binding site for C6. The C5b-C6 complex is the foundation upon which the lytic complex is assembled. Defects in C5 are the cause of complement component 5 deficiency (C5D). A rare defect of the complement classical pathway associated with susceptibility to severe recurrent infections, predominantly by Neisseria gonorrhoeae or Neisseria meningitidis. An association study of C5 haplotypes and genotypes in individuals with chronic hepatitis C virus infection shows that individuals homozygous for the C5_1 haplotype have a significantly higher stage of liver fibrosis than individuals carrying at least 1 other allele (PubMed:15995705). Protein type: Secreted, signal peptide; Secreted. Chromosomal Location of Human Ortholog: 9q33-q34. Cellular Component: membrane attack complex; extracellular space; extracellular region. Molecular Function: protein binding; chemokine activity; endopeptidase inhibitor activity; C5a anaphylatoxin chemotactic receptor binding; receptor binding. Biological Process: activation of MAPK activity; in utero embryonic development; positive regulation of chemotaxis; cytolysis; complement activation, alternative pathway; glucose homeostasis; chemotaxis; leukocyte migration during inflammatory response; complement activation; cellular calcium ion homeostasis; G-protein coupled receptor protein signaling pathway; positive regulation of angiogenesis; cell surface receptor linked signal transduction; regulation of complement activation; innate immune response; response to stress; inflammatory response; negative regulation of dopamine secretion; complement activation, classical pathway. Disease: Complement Component 5 Deficiency; Eculizumab, Poor Response To

48-Strip-Wells-(Competitive)

470 USD

48-Strip-Wells-(Sandwich)

470

96-Strip-Wells-(Competitive)

675

96-Strip-Wells-(Sandwich)

675