Structural highlights
Disease
UROK_HUMAN Defects in PLAU are the cause of Quebec platelet disorder (QPD) [MIM:601709. 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.[1]
Function
UROK_HUMAN Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.
Publication Abstract from PubMed
TXA is an active-site inhibitor of uPA. TXA attenuates MDA-MB-231 BAG cell migration and inhibits endogenous uPA activity.
Tranexamic acid is an active site inhibitor of urokinase plasminogen activator.,Wu G, Mazzitelli BA, Quek AJ, Veldman MJ, Conroy PJ, Caradoc-Davies TT, Ooms LM, Tuck KL, Schoenecker JG, Whisstock JC, Law RHP Blood Adv. 2019 Mar 12;3(5):729-733. doi: 10.1182/bloodadvances.2018025429. PMID:30814058[2]
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
See Also
References
- ↑ Paterson AD, Rommens JM, Bharaj B, Blavignac J, Wong I, Diamandis M, Waye JS, Rivard GE, Hayward CP. Persons with Quebec platelet disorder have a tandem duplication of PLAU, the urokinase plasminogen activator gene. Blood. 2010 Feb 11;115(6):1264-6. doi: 10.1182/blood-2009-07-233965. Epub 2009, Dec 9. PMID:20007542 doi:10.1182/blood-2009-07-233965
- ↑ Wu G, Mazzitelli BA, Quek AJ, Veldman MJ, Conroy PJ, Caradoc-Davies TT, Ooms LM, Tuck KL, Schoenecker JG, Whisstock JC, Law RHP. Tranexamic acid is an active site inhibitor of urokinase plasminogen activator. Blood Adv. 2019 Mar 12;3(5):729-733. PMID:30814058 doi:10.1182/bloodadvances.2018025429
