|Application ||WB, E|
|Calculated MW||163291 Da|
|Antigen Region||1162-1192 aa|
|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 rabbits immunized with a KLH conjugated synthetic peptide between 1162-1192 amino acids from the C-terminal region of human A2M.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|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) is for research use only and not for use in diagnostic or therapeutic procedures.|
|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.|
|Tissue Location||Secreted in plasma.|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
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].
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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