Porcine Complement Fragment 3a ELISA Kit | C3a elisa kit

Porcine Complement Fragment 3a ELISA Kit

Cat. Num. AAA752100

• Gene Names: C3; ASP; C3a; C3b; AHUS5; ARMD9; CPAMD1; HEL-S-62p
• Reactivity: Porcine
• Synonyms: Complement Fragment 3a; Porcine Complement Fragment 3a ELISA Kit; C3a elisa kit

• Reactivity: Porcine

• Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate
• Assay Type: Sandwich
• Sensitivity: 0.1 ng/mL.
• Intended Uses: This C3a ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Porcine C3a. This ELISA kit for research use only, not for therapeutic applications!
• Preparation and Storage: Store all reagents at 2-8 degree C.

Typical Testing Data/Standard Curve (for reference only)

Related Product Information for C3a elisa kit

Principle of the assay: C3a ELISA kit applies the quantitative sandwich enzyme immunoassay technique. The microtiter plate has been pre-coated with a monoclonal antibody specific for C3a. Standards or samples are then added to the microtiter plate wells and C3a if present, will bind to the antibody pre-coated wells. In order to quantitatively determine the amount of C3a present in the sample, a standardized preparation of horseradish peroxidase (HRP)-conjugated polyclonal antibody, specific for C3a are added to each well to “sandwich” the C3a 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 C3a 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 C3a concentration in each sample is interpolated from this standard curve.

Product Categories/Family for C3a elisa kit

Immunology

NCBI and Uniprot Product Information

• NCBI GI #: 115298678
• NCBI GeneID: 718
• NCBI Accession #: NP_000055.2
• NCBI GenBank Nucleotide #: NM_000064.2
• Molecular Weight: 187,148 Da
• NCBI Official Full Name: complement C3
• NCBI Official Synonym Full Names: complement component 3
• NCBI Official Symbol: C3
• NCBI Official Synonym Symbols: ASP; C3a; C3b; AHUS5; ARMD9; CPAMD1; HEL-S-62p
• NCBI Protein Information: complement C3; prepro-C3; C3a anaphylatoxin; complement component C3; complement component C3a; complement component C3b; acylation-stimulating protein cleavage product; epididymis secretory sperm binding protein Li 62p; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1
• UniProt Protein Name: Complement C3
• UniProt Gene Name: C3
• UniProt Synonym Gene Names: CPAMD1; ASP
• UniProt Entry Name: CO3_HUMAN

NCBI Description

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]

Uniprot Description

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; Inhibitor; Secreted

Chromosomal Location of Human Ortholog: 19p13.3-p13.2

Cellular Component: extracellular space; extracellular region; plasma membrane

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 G-protein coupled receptor protein signaling pathway; positive regulation of type IIa hypersensitivity; 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