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Monoclonal Mouse Anti-Human β-Amyloid, Clone 10H3 (90216)

  发布日期:2010/11/9 11:13:44   浏览次数:625
北京派胜医药科技有限公司
Beijing Pason Pharmaceuticals Inc.
Tel:  (8610) 68341662/63
Fax: (8610) 68341665
Presentation
This mouse monoclonal anti-human β-amyloid is supplied in PBS, sterile filtered (0.22μm) and without addition of preservatives.
Source
Mouse myeloma SP2/0 cells were fused with spleen cells of a Balb/c mouse immunized intraperitoneally with a synthetic peptide of 20 amino acids of the corresponding A4 sequence (1-3). This antibody has been purified from serum-free supernatant by protein A affinity chromatography.
Purity
The final product is more than 95% pure as determined by SDS-PAGE.
Applications
This antibody can be used for immunohistochemical staining, Western blot, ELISA techniques and in vivo imaging (4).
Specificity
This antibody recognizes all forms of β-amyloid and does not depend on N- or C-terminus ofr its reactivity.
Instructions for use
1. For immunohistochemistry: use this antibody in a concentration range of 5-10 μg/ml for the localization of β-amyloid in formalin-fixed, paraffinembedded brain tissue.
2. For Western blot: a final concentration of 1-5μg/ml can detect 50ng of SDS-denaturated and β-mercaptoethanol β-amyloid.
3. For ELISA: this antibody can be used at a


concentration of 5-10μg/ml as a ccapturing reagent for β-amyloid in a sandwich ELISA.


Note: The recommended concentrations are approximate values. For each application, a dose-response assay should be performed to determine the optimal concentration for use.
Storage and stability
Monoclonal mouse anti-β-amyloid, as shipped, is stable for at least six months when stored at -20℃. Avoid multiple freeze/thaw cycles by storage in appropriate aliquots.
This antibody should be diluted with PBS or medium containing a suitable carrier protein (e.g. 0.1 to 1% BSA). Failure to add carrier protein to diluted product will result in loss of activity.
References
(1)    Majocha RE, et al. Proc Natl Acad USA Sci 1988; 85: 6182-6.
(2)    Marotta CA, et al. Proc Natl Acad USA Sci 1989; 86: 337-41.
(3)    Tate-Ostroff B, et al. J Geriatr Psychiatry Neurol 1990; 3: 139-45.
(4)    Majocha RE, et al. J Nucl Med 1992; 33: 2184-9.
(5)    Maestre GE, et al. Brain Res 1992; 599: 64-72.
(6)    Frideland RP, et al. Mol Neurobiol 1994; 9: 107-13.
(7)    Friedland RP, et al. Ann MY Acad Sci 1997; 826: 242-7.

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