Product Description
Size: 50µg
Anti-C3 antibody [11H9] (ab11862) is a rat monoclonal antibody detecting C3/C3b in ICC/IF . Suitable for Mouse . - Over 50 publications - Trusted since 2004
Key facts
Host species:Rat,
Clonality:Monoclonal,
Clone number:11H9,
Isotype:IgG2a,
Carrier free:No,
Reacts with:Mouse,
Applications:ICC/IFSee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Immunogen:Cell preparation containing C3 protein. The exact immunogen used to generate this antibody is proprietary information.P01027,
Specificity:This antibody recognizes both intact C3 and its cleaved products C3b, iC3b, C3d and C3dg.The mature protein C3 has a molecular weight of approximately 190 kDa. The complement factor C3 consists of an alpha- and a beta-chain, linkedby disulfide bond. C3 convertase activates C3 by cleaving the alpha chain, releasing C3a anaphylotoxin and generating C3b (alpha chain and beta chain). C3b has a molecular weight of approximately 185 kDa. C3b is rapidly split in two positions by factor I and a cofactor to formiC3b (inactivated C3b) and C3f which is released. iC3b has a molecular weight of approximately 182 kDa. Does not cross react with C4.
Product details:
What is this antibody validated in?
Anti-C3 antibody [11H9] (ab11862) is a rat monoclonal antibody and is validated for use in Immunocytochemistry/immunofluorescence (ICC/IF) in Mouse samples.
Trusted by the scientific community
Anti-C3 [11H9] (ab11862) was first used in a scientific publication in 2004 and has been cited over 50 times in peer-reviewed journals.
Properties and Storage Information:
Form-Liquid, Purification technique-Affinity purification Protein G, Purification notes-0.2 µm filtered, Storage buffer-Preservative: 0.02% Sodium azideConstituents: PBS, 0.1% BSA, Shipped at conditions-Blue Ice, Appropriate short-term storage conditions-+4°C, Appropriate long-term storage conditions--20°C, Aliquoting information-Upon delivery aliquot, Storage information-Avoid freeze / thaw cycle
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Complement component 3 (C3) commonly known as C3 complement is a central protein in the complement system which plays a significant role in immune response. C3b a fragment of C3 is produced when C3 undergoes cleavage. C3 is a large protein with a mass of approximately 185 kDa. The liver primarily secretes C3 into the bloodstream. It circulates in the plasma and is found in high concentration making it one of the most abundant components of the complement system.
Biological function summary
Complement component C3 forms part of the innate immune system by promoting opsonization which enhances phagocytosis of pathogens. C3b binds to pathogens' surfaces facilitating their recognition by phagocytes. C3 as part of a complex with C3 convertase also has a role in amplifying the activation of the complement cascade. The proteolytic cleavage of C3 into C3b and C3a leads to the activation of other components forming the membrane attack complex and orchestrating inflammation.
Pathways
The complement component C3 functions within both the classical and alternative complement pathways. It acts as a convergence point where the complement activation pathways meet. C3 is activated into C3b and C3a which are key to amplifying the cascade. Furthermore C3 interacts with proteins such as factor B and factor D in the alternative pathway and C4 and C2 in the classical pathway facilitating the formation of C3 convertase necessary for pathway progression.
Complement C3 shows associations with immune-related and inflammatory diseases. Deficiencies or malfunctions of complement C3 can lead to increased susceptibility to infections due to impaired opsonization and clearance of pathogens. Additionally overactivation of the complement system involving C3 can contribute to autoimmune disorders such as systemic lupus erythematosus. Other proteins linked to these diseases include C4 in lupus and factor H in age-related macular degeneration which controls complement pathway activation.
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Collaboration
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