C8788
Complement C3 deficient serum human
substrate serum for C3 activity
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About This Item
UNSPSC Code:
12352200
NACRES:
NA.32
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General description
Complement C3 deficient serum is a normal human serum in which C3 protein is removed by affinity chromatography. Depleted serum helps in the complement cascade up to the preferred convertase level. It eases the formation of enzyme complex from purified components.
Application
Complement C3 deficient serum human has been used:
- as a component of the culture medium to study the influence of the inhibition of complement activation on complement receptors (CR3 and C3aR) expression in CD3+CD56+NKT-like cells
- as a negative control to evaluate the downstream complement activation post-mannan-binding lectin (MBL) pathway activation
- to study the opsonization of foreign particles by complement system
Physical form
Supplied as a solution in phosphate buffered saline, pH 7.4
Analysis Note
C3 is depleted by immunoadsorption as judged by a highly sensitive hemolytic assay.
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
10 - Combustible liquids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
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Marcin Okroj et al.
PloS one, 7(10), e47245-e47245 (2012-10-17)
C3 and C5 convertases are central stages of the complement cascade since they converge the different initiation pathways, augment complement activation by an amplification loop and lead to a common terminal pathway resulting in the formation of the membrane attack
Shin Yong Park et al.
Journal of immunology (Baltimore, Md. : 1950), 181(9), 6328-6336 (2008-10-23)
Enterococcus faecalis (Ef) accounts for most cases of enterococcal bacteremia, which is one of the principal causes of nosocomial bloodstream infections (BSI). Among several virulence factors associated with the pathogenesis of Ef, an extracellular gelatinase (GelE) has been known to
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