5hgg
From Proteopedia
(Difference between revisions)
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| - | '''Unreleased structure''' | ||
| - | + | ==Crystal structure of uPA in complex with a camelid-derived antibody fragment== | |
| - | + | <StructureSection load='5hgg' size='340' side='right' caption='[[5hgg]], [[Resolution|resolution]] 1.97Å' scene=''> | |
| - | + | == Structural highlights == | |
| - | + | <table><tr><td colspan='2'>[[5hgg]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5HGG OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5HGG FirstGlance]. <br> | |
| - | + | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=MES:2-(N-MORPHOLINO)-ETHANESULFONIC+ACID'>MES</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>, <scene name='pdbligand=TWN:(3S)-3-[(2S,3S,4R)-3,4-DIMETHYLTETRAHYDROFURAN-2-YL]BUTYL+LAURATE'>TWN</scene></td></tr> | |
| - | [[Category: | + | <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=5hgg FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5hgg OCA], [http://pdbe.org/5hgg PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5hgg RCSB], [http://www.ebi.ac.uk/pdbsum/5hgg 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: Kromann-Hansen, T]] | [[Category: Kromann-Hansen, T]] | ||
| - | [[Category: Ngo, J | + | [[Category: Ngo, J C.K]] |
| - | [[Category: | + | [[Category: Yung, K W.Y]] |
| - | [[Category: | + | [[Category: Hydrolase-inhibitor complex]] |
| + | [[Category: Nanobody]] | ||
| + | [[Category: Serine protease]] | ||
| + | [[Category: Upa]] | ||
Revision as of 06:08, 2 June 2016
Crystal structure of uPA in complex with a camelid-derived antibody fragment
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