The Monkey PAI-1 (SERPINE1) ELISA quantitates Rhesus Mk PAI-1 in monkey serum, plasma, or cell culture medium. The assay will exclusively recognize both natural and recombinant Mk PAI-1. Principle of the method The Monkey PAI-1 solid-phase sandwich ELISA (enzyme-linked immunosorbent assay) is designed to measure the amount of the target bound between a matched antibody pair. A target-specific antibody has been pre-coated in the wells of the supplied microplate. Samples, standards, or controls are then added into these wells and bind to the immobilized (capture) antibody. The sandwich is formed by the addition of the second (detector) antibody, a substrate solution is added that reacts with the enzyme-antibody-target complex to produce measurable signal. The intensity of this signal is directly proportional to the concentration of target present in the original specimen. Rigorous validation Each manufactured lot of this ELISA kit is quality tested for criteria such as sensitivity, specificity, precision, and lot-to-lot consistency. See manual for more information on validation.PAI1 (plasminogen activator inhibitor 1) belongs to serine protease inhibitor superfamily, and is the principal inhibitor of tissue-type and urokinase-type plasminogen activators (tPA and uPA). Platelets are the main source of the circulating PAI11, but it is synthesized and secreted by many tissue and cell types, including fibroblasts, smooth muscle cells, endothelial cells, hepatocytes, and inflammatory cells. Expression of PAI11 can be regulated at the transcriptional level by many factors including growth factors, cytokines, hormones, inflammatory factors, glucose or lipid metabolites, vascular tone regulating factors, chemicals, and other environmental or physical factors. PAI1 is present at increased levels in various disease states, and has been linked to an increased occurrence of thrombosis in obesity, thrombophilia and the metabolic syndrome. Defects in PAI-1 are characterized by abnormal bleeding. PAI1 mediates inhibition of fibrinolysis by inhibiting the activity of plasminogen activator, and may promote neuronal survival. Other defects in PAI1 are the cause of plasminogen activator inhibitor-1 deficiency (PAI-1 deficiency). Alternatively spliced transcript variants encoding different isoforms of PAI1 have been found.
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