A synthetic peptide, corresponding to residues in Human Lipoprotein a.
WB: Human plasma lysate.
Mouse, Rat: We have preliminary internal testing data to indicate this antibody may not react with these species. Please contact us for more information.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents
We are constantly working hard to ensure we provide our customers with best in class antibodies. As a result of this work we are pleased to now offer this antibody in purified format. We are in the process of updating our datasheets. The purified format is designated 'PUR' on our product labels. If you have any questions regarding this update, please contact our Scientific Support team.
This product is a recombinant rabbit monoclonal antibody.
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C. Avoid freeze / thaw cycle.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
1/10000 - 1/50000. Detects a band of approximately 501 kDa (predicted molecular weight: 501 kDa).
Is unsuitable for Flow Cyt,ICC/IF or IHC-P.
Lipoprotein(a) (Lp(a)) is a lipoprotein subclass assembled in the blood from low density lipoprotein (LDL) molecules and apolipoprotein-a (apo-a). Lp(a) recruits inflammatory cells through interaction with Mac-1 integrin. High Lp(a) in blood is a risk factor for coronary heart disease, cerebrovascular disease, atherosclerosis, thrombosis, and stroke. Lp(a) concentrations may be affected by disease states, but are only moderately affected by diet, exercise and other environmental factors. Lipid-reducing drugs have no effect on Lp(a) concentration. High Lp(a) predicts risk of early atherosclerosis similar to high LDL, but in advanced atherosclerosis, Lp(a) is a risk factor independent of LDL, indicating a coagulant risk of plaque thrombosis. Apo(a) contains domains that are very similar to plasminogen (PLG). Lp(a) accumulates in the vessel wall and inhibits binding of PLG to the cell surface, reducing plasmin generation which increases clotting. This inhibition also promotes proliferation of smooth muscle cells. These unique features of Lp(a) suggest a role in the generation of clots and atherosclerosis.