ELISA/assay

Fish Complement Component 3 ELISA Kit

MBS005953

48-Strip-Wells

470 USD

ELISA Kit

Fish 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; 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 chainComplement C3 alpha chainC3a anaphylatoxinAcylation stimulating protein; ASP; Alternative name(s):; C3adesArg]

[C3]

[C3; C3; ASP; C3a; C3b; AHUS5; ARMD9; CPAMD1; CPAMD1; ASP]

CO3_HUMAN

Fish

No significant cross-reactivity or interference between this analyte and analogues is observed.

Store all reagents at 2-8 degree C

Samples: Human Body Fluids, Tissue Homogenates, Secretions Or Feces Samples. Assay Type: Quantitative Sandwich. Detection Range: 3.12 ng/ml-100 ng/ml. Sensitivity: 1.0 ng/ml.

Intra-assay Precision: Intra-assay CV (%) is less than 15%. Inter-assay Precision: Inter-assay CV (%) is less than 15%. [CV(%) = SD/mean ×100].

Background/Introduction: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! This kit is intended to be used for determination the level of C20ORF39 (hereafter termed "analyte") in undiluted original Human body fluids, tissue homogenates, secretions or feces samples. This kit is NOT suitable for assaying non-biological sources of substances.

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. 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: Secreted, signal peptide; Secreted; Inhibitor. 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; 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

680

5x96-Strip-Wells

3100

10x96-Strip-Wells

6095