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物種交叉反應(yīng)性
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Human, porcine. 7 No cross-reactivity was observed with specimens from baboon, bovine, cat, chicken, dog, guinea pig, hamster, horse, mouse, rabbit, rat, or sheep
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背景
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Activation of the classical complement pathway begins with the binding of an activating substance (e.g. immune complex) to the C1q molecule of C1. This, in turn, activates the C1r(2)C1s(2) sub-units, resulting in cleavage of C4 to C4b near the amino terminus of the gamma chain releasing C4a in the process. The short-lived C4b molecule can bind covalently to membranes or other surfaces via either an amide or ester bond. This is an inefficient process that is limited to the immediate vicinity of the C1 complex. C4b then takes part in the classical convertase enzyme. Because of the short life of the C4b molecule much of the C4d is free and circulates in serum.
Both bound and free C4b are strictly controlled in vivo. The ability of C4b to participate in classical pathway activation and opsonization reactions is inhibited by a single site cleavage of the alpha chain by Factor I. This reaction requires either C4 binding protein or CR1 as a cofactor. This initial cleavage inactivates C4b resulting in iC4b. Further degradation of this molecule by Factor I produces the C4c and C4d fragments. Both of these fragments can be produced in fluid phase or on target surface.
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特異性
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The specificity of the monoclonal antibody was established via a series of immunoassays. The antibody was shown by ELISA to bind highly purified C4d and intact C4, but not to purified C4c. Additionally, the antibody was shown to immunoprecipitate the C4d fragment using radiolabeled C4d with protein A-bearing bacteria, but not the C4c fragment.
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應(yīng)用
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Because specific techniques differ from lab to lab, the provided information should be used as a guideline only. As C4b has a short half life in vivo, C4d is an excellent marker for classical complement activation in vivo or in vitro and is therefore the basis of the MicroVue C4d EIA Kit (Cat. #A008).
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參考文獻
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1、Rogers, J., Cooper, N., et al. Complement Activation by ?-amyloid in Alzheimer disease, PNAS 89:10016-10020, 1992.
2、Schwab, C. Steele, J.C. McGeer, P.L. Neurofibrillary tangles of Guam parkinson-dementia are associated with reactive microglia and complement proteins, Brain Res. 707(2):196-204, 1996.
3、Gemmell, C. A flow cytometric immunoassay to quantify adsorption of complement activation products on artificial surfaces, J Biomed Mater Res 37, 474-480, 1997.
4、Solzner, S., Lemerre, C. et al. Temporal accural of complement proteins in Amyloid plaques in patients with Down syndrome with Alzheimer's Disease, Am J Path 156:489-499, 2000.
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