Home \ Antibodies \ C3b, iC3b, C3c, Human, clone C3-42.3
Catalog # HM2394

C3b, iC3b, C3c, Human, clone C3-42.3

120,00375,00

Please choose the quantity of items you wish to add to your cart…

The antibody clone C3-42.3 recognize complement C3, C3b, iC3b and C3c. The recognition domain is determined to MG4/5. The antibody blocks C3 activation by AP C3-convertase. The complement system plays important roles in both innate and adaptive immune response and can produce an inflammatory and protective reaction to challenges from pathogens before an adaptive response can occur. It consists of a complex family of proteins and receptors which are found in the circulation, in tissues and other body-fluids. There are three pathways of complement activation. The classical pathway is initiated by Immune complexes; the lectin pathway by surface bound lectins; and the AP by all the surfaces that are not specifically protected against it. Each generates a C3 convertase, a serine protease that cleaves the central complement protein C3, and generates the major cleavage fragment C3b. The C3 and C5 convertases are enzymatic complexes that initiate and amplify the activity of the complement pathways and ultimately generate the cytolytic MAC. The synthesis of C3 is tissue-specific and is modulated in response to a variety of stimulatory agents. After cleavage by C3 convertase the anaphylotoxin C3a and activating C3b are formed. When bound to the cell surface C3b forms the start of the terminal pathway of complement by initiating the formation of the C5 convertase. C3 has a molecular weight of app. 185kDa and is the most abundant protein of the complement system with serum protein levels of about 1.3 mg/ml. C3 is primarily produced by the liver but is also generated in macrophages, neutrophils, endothelial and epithelial cells. Due to the high levels in circulation with low biological reactivity, C3 is able to act in a fast and potent way when danger by e.g. pathogens is encountered. Defects in C3 can be unfavorable to the host leading to recurrent infections or auto-immune diseases. Although rare, C3 deficiency has been reported. These patients suffer from recurrent infections of eg S.pneumoniae or N.meningitidis due to lack of opsonization, but also impaired DC and Treg development. Polymorphism in C3 has been associated with AMD and aHUS. Besides clearance of pathogens, C3 is also important in removal of circulating immune-complexes by assisting the phagocytic capacity of macrophages. Malfunction of this system can lead to development of auto-immune disease and complement deposition in tissues.

Application
Functional studies, Immuno assays, Western blot

Application Notes
• IA: antibody C3-42.3 was used in a direct ELISA.
• FS: the antibody blocks C3 activation by alternative pathway C3-convertase (Ref.1)
• W: the antibody is used under reduced conditions. Expected band size is 71 kDa.

Product type
Monoclonal antibodies
Quantity
20 µg, 100 µg
Formulation
0.2 µm filtered in PBS+0.1%BSA
Immunogen
Mixture of the human activated C3 fragments, C3b, iC3b, and C3dg, emulsified in complete Freund’s adjuvant. Subsequently, mice were boosted three times at 2-week intervals with the same amount of
Isotype
Mouse IgG2b
Species
Human
Alias
Complement component C3b, iC3b, C3c
Storage and stability
Product should be stored at 4°C. Under recommended storage conditions, product is stable for at least one year.
Precautions
For research use only. Not for use in or on humans or animals or for diagnostics. It is the responsibility of the user to comply with all local/state and federal rules in the use of this product. Hycult Biotech is not responsible for any patent infringements that might result from the use or derivation of this product.
CoA-TDS HM2300-HM2400

Calculate your ELISA data easily

With the ELISA calculator you can easily calculate ELISA data. Assayfit Pro helps to perform curve fitting. The calculator generates advanced reports, fit graph, fit parameters and goodness of fit are shown.

Hycultbiotech_contact us

Would you like some virtual coffee?

Contact us