C0913
Complement C2 deficient serum human
for complement assays
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About This Item
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Application
C2 is a critical protease for compliment activation, which supports bacterial killing via phagocytes. C2 can be used in research to explore the mechanisms by which bacterial pathogens evade detection by the compliment system. One such mechanism by the bacteria Pseudomonas aeruginosa, uses the alkaline protease (AprA) to degrade and cleave C2 which ultimately interferes with the classical and lectin pathways. Research has shown that C2 deficiency results in an increased risk of infection by Streptococcus pyogenes through impaired phaogocytosis and neutrophil dependent killing.
Biochem/physiol Actions
Heritable complement C2 deficiency can manifest as a number of severe dermatological disorders, including discoid lupus erythematosus, idiopathic atrophoderma, and dermatomyositis.
Physical form
Supplied as a solution in PBS, pH 7.2
Analysis Note
C2 is depleted by immunoadsorption method as judged by a highly sensitive hemolytic assay and Ouchterlony immunodiffusion method.
Disclaimer
RESEARCH USE ONLY. This product is regulated in France when intended to be used for scientific purposes, including for import and export activities (Article L 1211-1 paragraph 2 of the Public Health Code). The purchaser (i.e. enduser) is required to obtain an import authorization from the France Ministry of Research referred in the Article L1245-5-1 II. of Public Health Code. By ordering this product, you are confirming that you have obtained the proper import authorization.
Storage Class
12 - Non Combustible Liquids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificados de análisis (COA)
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Pseudomonas aeruginosa Alkaline Protease Blocks Complement Activation via the Classical and Lectin Pathways.
Journal of Immunology (2011)
Developmental and comparative immunology, 26(6), 533-541 (2002-05-29)
Complement factor B and C2 are two critical proteases for complement activation. Some bony fish have been reported to possess duplicated genes for B/C2, but there is no direct evidence regarding possible functional divergence. Here, we report the isolation of
The American journal of medicine, 58(1), 83-91 (1975-01-01)
A 60 year old white man in previous good health presented with a 6 month history of progressive muscle weakness. Clinical and laboratory findings were typical of dermatomyositis. Muscle biopsy confirmed the presence of inflammatory myopathy; deposits of immunoglobulin G
Cryo-EM structures of Trypanosoma brucei gambiense ISG65 with human complement C3 and C3b and their roles in alternative pathway restriction.
Nature Communications, 14, 2403-2403 (2023)
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