View source for 4zko


==The crystal structure of upain-1-W3A in complex with uPA at pH7.4==
<StructureSection load='4zko' size='340' side='right'caption='[[4zko]], [[Resolution|resolution]] 1.29&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[4zko]] is a 3 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ZKO OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4ZKO FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=P6G:HEXAETHYLENE+GLYCOL'>P6G</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[4zkn|4zkn]], [[4zkr|4zkr]], [[4zks|4zks]]</td></tr>
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">PLAU ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/U-plasminogen_activator U-plasminogen activator], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.4.21.73 3.4.21.73] </span></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4zko FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4zko OCA], [http://pdbe.org/4zko PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4zko RCSB], [http://www.ebi.ac.uk/pdbsum/4zko PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4zko ProSAT]</span></td></tr>
</table>
== 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. 

==See Also==
*[[Plasminogen activator|Plasminogen activator]]
*[[Urokinase|Urokinase]]
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Human]]
[[Category: Large Structures]]
[[Category: U-plasminogen activator]]
[[Category: Andreasen, P A]]
[[Category: Huang, M]]
[[Category: Jiang, L]]
[[Category: Hydrolase-hydrolase inhibitor complex]]
[[Category: Peptides inhibitor]]
[[Category: Serine protease]]
[[Category: Upa]]