5wxf: Difference between revisions
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==Crystal structure of uPA in complex with upain-2-2== | |||
<StructureSection load='5wxf' size='340' side='right' caption='[[5wxf]], [[Resolution|resolution]] 1.46Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[5wxf]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5WXF OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5WXF FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr> | |||
[[Category: | <tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=HRG:L-HOMOARGININE'>HRG</scene></td></tr> | ||
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[5wxo|5wxo]], [[5wxp|5wxp]], [[5wxq|5wxq]], [[5wxr|5wxr]], [[5wxs|5wxs]], [[5wxt|5wxt]]</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=5wxf FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5wxf OCA], [http://pdbe.org/5wxf PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5wxf RCSB], [http://www.ebi.ac.uk/pdbsum/5wxf PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5wxf 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]] | |||