4zkn
From Proteopedia
(Difference between revisions)
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| - | '''Unreleased structure''' | ||
| - | The | + | ==The crystal structure of upain-1-W3A in complex with uPA at pH5.5== |
| - | + | <StructureSection load='4zkn' size='340' side='right' caption='[[4zkn]], [[Resolution|resolution]] 1.36Å' scene=''> | |
| - | + | == Structural highlights == | |
| - | + | <table><tr><td colspan='2'>[[4zkn]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ZKN OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4ZKN FirstGlance]. <br> | |
| - | + | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=PG4:TETRAETHYLENE+GLYCOL'>PG4</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr> | |
| - | [[Category: | + | <tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[4zko|4zko]], [[4zkr|4zkr]], [[4zks|4zks]]</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=4zkn FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4zkn OCA], [http://pdbe.org/4zkn PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4zkn RCSB], [http://www.ebi.ac.uk/pdbsum/4zkn PDBsum]</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: Andreasen, P A]] | ||
[[Category: Huang, M]] | [[Category: Huang, M]] | ||
[[Category: Jiang, L]] | [[Category: Jiang, L]] | ||
| - | [[Category: | + | [[Category: Hydrolase-hydrolase inhibitor complex]] |
| + | [[Category: Peptides inhibitor]] | ||
| + | [[Category: Serine protease]] | ||
| + | [[Category: Upa]] | ||
Revision as of 15:47, 1 June 2016
The crystal structure of upain-1-W3A in complex with uPA at pH5.5
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