4xsk

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'''Unreleased structure'''
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==Structure of PAItrap, an uPA mutant==
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<StructureSection load='4xsk' size='340' side='right' caption='[[4xsk]], [[Resolution|resolution]] 1.50&Aring;' scene=''>
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The entry 4xsk is ON HOLD until Feb 22 2017
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== Structural highlights ==
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<table><tr><td colspan='2'>[[4xsk]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4XSK OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4XSK FirstGlance]. <br>
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Authors: Gong, L., Proulle, V., Hong, Z., Lin, Z., Liu, M., Yuan, C., Lin, L., Furie, B., Flaumenhaft, R., Andreasen, P., Furie, B., Huang, M.
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</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=PGE:TRIETHYLENE+GLYCOL'>PGE</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
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<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>
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Description: Structure of PAItrap, an uPA mutant
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<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=4xsk FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4xsk OCA], [http://pdbe.org/4xsk PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4xsk RCSB], [http://www.ebi.ac.uk/pdbsum/4xsk PDBsum]</span></td></tr>
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[[Category: Unreleased Structures]]
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</table>
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== Disease ==
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[[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>
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== Function ==
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[[http://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN]] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.
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== References ==
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<references/>
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__TOC__
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</StructureSection>
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[[Category: U-plasminogen activator]]
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[[Category: Andreasen, P]]
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[[Category: Flaumenhaft, R]]
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[[Category: Furie, B]]
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[[Category: Gong, L]]
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[[Category: Hong, Z]]
[[Category: Huang, M]]
[[Category: Huang, M]]
[[Category: Lin, L]]
[[Category: Lin, L]]
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[[Category: Lin, Z]]
[[Category: Liu, M]]
[[Category: Liu, M]]
[[Category: Proulle, V]]
[[Category: Proulle, V]]
[[Category: Yuan, C]]
[[Category: Yuan, C]]
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[[Category: Lin, Z]]
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[[Category: Antagonist]]
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[[Category: Andreasen, P]]
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[[Category: Blood clotting]]
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[[Category: Flaumenhaft, R]]
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[[Category: Pai-1]]
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[[Category: Furie, B]]
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[[Category: Upa]]
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[[Category: Hong, Z]]
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[[Category: Gong, L]]
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Revision as of 15:50, 3 February 2016

Structure of PAItrap, an uPA mutant

4xsk, resolution 1.50Å

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