4xsk

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Current revision (15:30, 8 November 2023) (edit) (undo)
 
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<StructureSection load='4xsk' size='340' side='right'caption='[[4xsk]], [[Resolution|resolution]] 1.50&Aring;' scene=''>
<StructureSection load='4xsk' size='340' side='right'caption='[[4xsk]], [[Resolution|resolution]] 1.50&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
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<table><tr><td colspan='2'>[[4xsk]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. 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 [https://proteopedia.org/fgij/fg.htm?mol=4XSK FirstGlance]. <br>
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<table><tr><td colspan='2'>[[4xsk]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. 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 [https://proteopedia.org/fgij/fg.htm?mol=4XSK FirstGlance]. <br>
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</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><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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</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.5&#8491;</td></tr>
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<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">PLAU ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
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<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><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'>[https://en.wikipedia.org/wiki/U-plasminogen_activator U-plasminogen activator], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.4.21.73 3.4.21.73] </span></td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=4xsk FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4xsk OCA], [https://pdbe.org/4xsk PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4xsk RCSB], [https://www.ebi.ac.uk/pdbsum/4xsk PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4xsk ProSAT]</span></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=4xsk FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4xsk OCA], [https://pdbe.org/4xsk PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4xsk RCSB], [https://www.ebi.ac.uk/pdbsum/4xsk PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4xsk ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
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[[https://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN]] Defects in PLAU are the cause of Quebec platelet disorder (QPD) [MIM:[https://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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[https://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN] Defects in PLAU are the cause of Quebec platelet disorder (QPD) [MIM:[https://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 ==
== Function ==
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[[https://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN]] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.
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[https://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.
==See Also==
==See Also==
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__TOC__
__TOC__
</StructureSection>
</StructureSection>
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[[Category: Human]]
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[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Large Structures]]
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[[Category: U-plasminogen activator]]
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[[Category: Andreasen P]]
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[[Category: Andreasen, P]]
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[[Category: Flaumenhaft R]]
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[[Category: Flaumenhaft, R]]
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[[Category: Furie B]]
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[[Category: Furie, B]]
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[[Category: Gong L]]
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[[Category: Gong, L]]
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[[Category: Hong Z]]
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[[Category: Hong, Z]]
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[[Category: Huang M]]
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[[Category: Huang, M]]
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[[Category: Lin L]]
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[[Category: Lin, L]]
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[[Category: Lin Z]]
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[[Category: Lin, Z]]
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[[Category: Liu M]]
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[[Category: Liu, M]]
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[[Category: Proulle V]]
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[[Category: Proulle, V]]
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[[Category: Yuan C]]
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[[Category: Yuan, C]]
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[[Category: Antagonist]]
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[[Category: Blood clotting]]
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[[Category: Pai-1]]
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[[Category: Upa]]
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Current revision

Structure of PAItrap, an uPA mutant

PDB ID 4xsk

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