5wxt: Difference between revisions
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==Crystal structure of uPA-S195A in complex with S2444== | |||
<StructureSection load='5wxt' size='340' side='right' caption='[[5wxt]], [[Resolution|resolution]] 2.10Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[5wxt]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5WXT OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5WXT FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=7YR:(2R)-N-[2-[[(2S)-1-[[4-[bis(oxidanyl)amino]phenyl]amino]-5-carbamimidamido-1-oxidanylidene-pentan-2-yl]amino]-2-oxidanylidene-ethyl]-5-oxidanylidene-pyrrolidine-2-carboxamide'>7YR</scene></td></tr> | |||
[[Category: | <tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[5wxf|5wxf]], [[5wxo|5wxo]], [[5wxp|5wxp]], [[5wxq|5wxq]], [[5wxr|5wxr]], [[5wxs|5wxs]]</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=5wxt FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5wxt OCA], [http://pdbe.org/5wxt PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5wxt RCSB], [http://www.ebi.ac.uk/pdbsum/5wxt PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5wxt 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. | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: U-plasminogen activator]] | |||
[[Category: Huang, M]] | [[Category: Huang, M]] | ||
[[Category: Jiang, L]] | [[Category: Jiang, L]] | ||
[[Category: Hydrolase-hydrolase inhibitor complex]] | |||
[[Category: Pepetide inhibitor]] | |||
[[Category: Serine protease]] | |||
[[Category: Upa]] | |||