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{{STRUCTURE_4fuf|  PDB=4fuf  |  SCENE=  }}
===Crystal Structure of the Urokinase===


==Disease==
==Crystal Structure of the Urokinase==
[[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>  
<StructureSection load='4fuf' size='340' side='right'caption='[[4fuf]], [[Resolution|resolution]] 2.00&Aring;' scene=''>
 
== Structural highlights ==
==Function==
<table><tr><td colspan='2'>[[4fuf]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4FUF OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4FUF FirstGlance]. <br>
[[http://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN]] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2&#8491;</td></tr>
 
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=8UP:8-(3-BROMOPROPOXY)-7-METHOXYNAPHTHALENE-2-CARBOXIMIDAMIDE'>8UP</scene>, <scene name='pdbligand=ACT:ACETATE+ION'>ACT</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=SIN:SUCCINIC+ACID'>SIN</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
==About this Structure==
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=4fuf FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4fuf OCA], [https://pdbe.org/4fuf PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4fuf RCSB], [https://www.ebi.ac.uk/pdbsum/4fuf PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4fuf ProSAT]</span></td></tr>
[[4fuf]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4FUF OCA].  
</table>
== Disease ==
[https://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN] Defects in PLAU are the cause of Quebec platelet disorder (QPD) [MIM:[https://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 ==
[https://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.


==See Also==
==See Also==
*[[Urokinase|Urokinase]]
*[[Urokinase 3D Structures|Urokinase 3D Structures]]
 
== References ==
==Reference==
<references/>
<references group="xtra"/><references/>
__TOC__
</StructureSection>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: U-plasminogen activator]]
[[Category: Large Structures]]
[[Category: Giranda, V.]]
[[Category: Giranda V]]
[[Category: Kang, Y N.]]
[[Category: Kang YN]]
[[Category: Nienaber, V.]]
[[Category: Nienaber V]]
[[Category: Stuckey, J A.]]
[[Category: Stuckey JA]]
[[Category: Hydrolase]]
[[Category: Hydrolase-hydrolase inhibitor complex]]

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