PLAU Antibody – Rabbit Polyclonal

uPA: Specifically cleave the zymogen plasminogen to form the active enzyme plasmin. Defects in PLAU are the cause of Quebec platelet disorder (QPD). QPD is an autosomal dominant bleeding disorder due to a gain-of-function defect in fibrinolysis. Although affected individuals do not exhibit systemic fibrinolysis, they show delayed onset bleeding after challenge, such as surgery. The hallmark of the disorder is markedly increased PLAU levels within platelets, which causes intraplatelet plasmin generation and secondary degradation of alpha-granule proteins. Belongs to the peptidase S1 family. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Secreted, signal peptide; Protease; EC 3.4.21.73; Motility/polarity/chemotaxis; Secreted

Cellular Component: extracellular space; cell surface; focal adhesion; membrane

Molecular Function: peptidase activity; serine-type endopeptidase activity; kinase activity

Biological Process: wound healing; smooth muscle cell migration; skeletal muscle regeneration; positive regulation of smooth muscle cell migration; proteolysis; regulation of cell proliferation; fibrinolysis; regulation of cell adhesion mediated by integrin; response to hyperoxia; regulation of smooth muscle cell migration; positive regulation of cell proliferation; response to hypoxia; spermatogenesis; angiogenesis; regulation of receptor activity; response to activity; phosphorylation; embryo implantation