1lmw: Difference between revisions
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{{STRUCTURE_1lmw| PDB=1lmw | SCENE= }} | {{STRUCTURE_1lmw| PDB=1lmw | SCENE= }} | ||
===LMW U-PA Structure complexed with EGRCMK (GLU-GLY-ARG Chloromethyl Ketone)=== | |||
{{ABSTRACT_PUBMED_8591045}} | |||
=== | ==Disease== | ||
[[http://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN]] Defects in PLAU are the cause of Quebec platelet disorder (QPD) [MIM:[http://omim.org/entry/601709 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.<ref>PMID:20007542</ref> | |||
==Function== | |||
[[http://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN]] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin. | |||
==About this Structure== | ==About this Structure== | ||
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==Reference== | ==Reference== | ||
<ref group="xtra">PMID:008591045</ref><references group="xtra"/> | <ref group="xtra">PMID:008591045</ref><references group="xtra"/><references/> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: U-plasminogen activator]] | [[Category: U-plasminogen activator]] | ||