PAI1 Mouse anti-Human, Clone: 242816, Invitrogen
Mouse Monoclonal Antibody
Manufacturer: Invitrogen MA523790
In direct ELISAs, no cross-reactivity with Recombinant human Serpin A1, A3, A4, A8, C1, F1, F2, I1, I2, Recombinant mouse Serpin D1 or E2 is observed. Reconstitute at 0.5 mg/mL in sterile PBS.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.
|PBS with 5% trehalose and No Preservative|
|PAI, PAI-1, PAI1, PLANH1, SERPINE-1|
|-20° C, Avoid Freeze/Thaw Cycles|
|ELISA, Neutralization, Western Blot|
|Sf 21-derived recombit human Serpin E1/PAI-1 Met1-Pro402|
We continue to work to improve your shopping experience and your feedback regarding this content is very important to us. Please use the form below to provide feedback related to the content on this product.
Your feedback has been submitted. Fisher Scientific is always working to improve our content for you. We appreciate your feedback.Ok