4xsk: Difference between revisions
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<StructureSection load='4xsk' size='340' side='right'caption='[[4xsk]], [[Resolution|resolution]] 1.50Å' scene=''> | <StructureSection load='4xsk' size='340' side='right'caption='[[4xsk]], [[Resolution|resolution]] 1.50Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[4xsk]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/ | <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> | ||
</td></tr><tr id=' | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.5Å</td></tr> | ||
<tr id=' | <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> | ||
< | |||
<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 == | ||
[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 == | ||
[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> | ||
[[Category: | [[Category: Homo sapiens]] | ||
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
[[Category: Andreasen P]] | |||
[[Category: Andreasen | [[Category: Flaumenhaft R]] | ||
[[Category: Flaumenhaft | [[Category: Furie B]] | ||
[[Category: Furie | [[Category: Gong L]] | ||
[[Category: Gong | [[Category: Hong Z]] | ||
[[Category: Hong | [[Category: Huang M]] | ||
[[Category: Huang | [[Category: Lin L]] | ||
[[Category: Lin | [[Category: Lin Z]] | ||
[[Category: Lin | [[Category: Liu M]] | ||
[[Category: Liu | [[Category: Proulle V]] | ||
[[Category: Proulle | [[Category: Yuan C]] | ||
[[Category: Yuan | |||
Latest revision as of 18:30, 8 November 2023
Structure of PAItrap, an uPA mutantStructure of PAItrap, an uPA mutant
Structural highlights
DiseaseUROK_HUMAN Defects in PLAU are the cause of Quebec platelet disorder (QPD) [MIM: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.[1] FunctionUROK_HUMAN Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin. See AlsoReferences
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