ELISA/assay

Cavy Complement Component 5a ELISA Kit

MBS053051

48-Strip-Wells

470 USD

ELISA Kit

Cavy Complement Component 5a ELISA Kit

[Complement Component 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 4]

[C5a]

[C5; C5; C5D; C5a; C5b; ECLZB; CPAMD4; CPAMD4]

CO5_HUMAN

Cavy

1676

Store all reagents at 2-8 degree C

38016947

NP_001726.2

NM_001735.2

P01031

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; Secreted, signal peptide. 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

680

5x96-Strip-Wells

3100

10x96-Strip-Wells

6095