ELISA/assay

Monkey Complement fragment 5a ELISA Kit

MBS755465

48-Strip-Wells

470 USD

ELISA Kit

Monkey Complement fragment 5a ELISA Kit

Complement fragment 5a

complement C5 preproprotein; 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

C5a

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

CO5_HUMAN

Monkey

This assay has high sensitivity and excellent specificity for detection of C5a. No significant cross-reactivity or interference between C5a and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between C5a 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 C5a ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Monkey C5a. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Immunology

Priciple of the assay: C5a ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-C5a antibody and an C5a-HRP conjugate. The assay sample and buffer are incubated together with C5a-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 C5a concentration since C5a from samples and C5a-HRP conjugate compete for the anti-C5a antibody binding site. Since the number of sites is limited, as more sites are occupied by C5a from the sample, fewer sites are left to bind C5a-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The C5a concentration in each sample is interpolated from this standard curve.

38016947

NP_001726.2

NM_001735.2

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; positive regulation of chemotaxis; in utero embryonic development; cytolysis; complement activation, alternative pathway; chemotaxis; glucose homeostasis; 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; response to stress; innate immune response; inflammatory response; negative regulation of dopamine secretion; complement activation, classical pathway. Disease: Complement Component 5 Deficiency; Eculizumab, Poor Response To

48-Strip-Wells

470 USD

96-Strip-Wells

675