A2M Antibody (C-term) (Ascites)
Mouse Monoclonal Antibody (Mab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, E |
---|---|
Primary Accession | P01023 |
Other Accession | NP_000005 |
Reactivity | Mouse |
Host | Mouse |
Clonality | Monoclonal |
Isotype | IgM |
Clone/Animal Names | 590CT15.5.5 |
Calculated MW | 163291 Da |
Antigen Region | 1162-1192 aa |
Gene ID | 2 |
---|---|
Other Names | Alpha-2-macroglobulin, Alpha-2-M, C3 and PZP-like alpha-2-macroglobulin domain-containing protein 5, A2M, CPAMD5 |
Target/Specificity | This A2M antibody is generated from mice immunized with a KLH conjugated synthetic peptide between 1162-1192 amino acids from the C-terminal region of human A2M. |
Dilution | WB~~1:500~1000 |
Format | Mouse monoclonal antibody supplied in crude ascites with 0.09% (W/V) sodium azide. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | A2M Antibody (C-term) (Ascites) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | A2M |
---|---|
Synonyms | CPAMD5 |
Function | Is able to inhibit all four classes of proteinases by a unique 'trapping' mechanism. This protein has a peptide stretch, called the 'bait region' which contains specific cleavage sites for different proteinases. When a proteinase cleaves the bait region, a conformational change is induced in the protein which traps the proteinase. The entrapped enzyme remains active against low molecular weight substrates (activity against high molecular weight substrates is greatly reduced). Following cleavage in the bait region, a thioester bond is hydrolyzed and mediates the covalent binding of the protein to the proteinase. |
Cellular Location | Secreted. |
Tissue Location | Secreted in plasma.. |
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Background
Alpha-2-macroglobulin is a protease inhibitor and cytokine transporter. It inhibits many proteases, including trypsin, thrombin and collagenase. A2M is implicated in Alzheimer disease (AD) due to its ability to mediate the clearance and degradation of A-beta, the major component of beta-amyloid deposits. [provided by RefSeq].
References
Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)
Bruno, E., et al. Neurosci. Lett. 482(2):112-116(2010)
Nalpas, B., et al. Gut 59(8):1120-1126(2010)
Song, H., et al. Neurosci. Lett. 479(2):143-145(2010)
Seriramalu, R., et al. Electrophoresis 31(14):2388-2395(2010)
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