ELISA/assay

Human C3a (Complement Component 3a) ELISA Kit

MBS2513669

24-Strip-Wells

215 USD

ELISA Kit

Human C3a (Complement Component 3a) ELISA Kit

[C3a]

[complement C3; Complement C3; complement C3; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1; C3a anaphylatoxin; acylation-stimulating protein cleavage product; complement component C3; complement component C3a; complement component C3b; epididymis secretory sperm binding protein Li 62p; prepro-C3; complement component 3; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1Cleaved into the following 12 chains:Complement C3 beta chain; C3-beta-c; C3bc; Complement C3 alpha chain; C3a anaphylatoxin; Acylation stimulating protein; ASPAlternative name(s):C3adesArg]

[C3a]

[C3; C3; ASP; C3a; C3b; AHUS5; ARMD9; CPAMD1; HEL-S-62p; CPAMD1; C3bc; ASP]

CO3_HUMAN

Human

1663

This kit recognizes natural and recombinantHumanC3a. No significant cross-reactivity or interference between HumanC3a and analogues was observed.

Store at 4 degree C.

Typical Testing Data/Standard Curve (for reference only)

Samples: Serum, Plasma, Biological Fluids. Assay Type: Sandwich. Detection Range: 0.313-20ng/mL. Sensitivity: Min: 0.188ng/mL; Max: 20ng/mL

Intended Uses: This ELISA kit applies to the invitro quantitative determination of HumanC3aconcentrations in serum, plasma and other biological fluids. Principle of the Assay: This ELISA kit uses Sandwich-ELISA as the method. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to C3a. Standards or samples are added to the appropriate micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for C3aand Avidin-Horseradish Peroxidase (HRP) conjugate is added to each micro plate well successively and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain C3a, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of a sulphuric acid solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm +/- 2 nm. The OD value is proportional to the concentration of C3a.You can calculate the concentration of C3ain the samples by comparing the OD of the samples to the standard curve.

115298678

NP_000055.2

NM_000064.3

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. A peptide (C3a) derived from the encoded protein has antimicrobial activity, so people with C3 deficiency are susceptible to bacterial infection. [provided by RefSeq, Nov 2014]

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; Inhibitor; Secreted, signal peptide. 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; signal transduction; fatty acid metabolic process; 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

24-Strip-Wells

215 USD

48-Strip-Wells

410

96-Strip-Wells

490

5x96-Strip-Wells

2040

10x96-Strip-Wells

3590