Plau blocking peptide
Mouse Plau Blocking Peptide (C-term)
NCBI and Uniprot Product Information
Uniprot Description
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: Motility/polarity/chemotaxis; EC 3.4.21.73; Protease; Secreted; Secreted, signal peptide
Cellular Component: cell surface; extracellular space; focal adhesion; membrane
Molecular Function: peptidase activity; protein binding; serine-type endopeptidase activity
Biological Process: angiogenesis; fibrinolysis; positive regulation of cell migration; positive regulation of cell proliferation; positive regulation of smooth muscle cell migration; proteolysis; regulation of cell adhesion mediated by integrin; regulation of cell proliferation; regulation of receptor activity; regulation of smooth muscle cell migration; response to hypoxia; skeletal muscle regeneration; smooth muscle cell migration; wound healing