5wxr: Difference between revisions
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<StructureSection load='5wxr' size='340' side='right'caption='[[5wxr]], [[Resolution|resolution]] 1.75Å' scene=''> | <StructureSection load='5wxr' size='340' side='right'caption='[[5wxr]], [[Resolution|resolution]] 1.75Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[5wxr]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5WXR OCA]. For a <b>guided tour on the structure components</b> use [ | <table><tr><td colspan='2'>[[5wxr]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Phage_display_vector_pTDisp Phage display vector pTDisp]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5WXR OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5WXR 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]] 1.75Å</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=5wxr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5wxr OCA], [https://pdbe.org/5wxr PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5wxr RCSB], [https://www.ebi.ac.uk/pdbsum/5wxr PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5wxr ProSAT]</span></td></tr> | |||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | |||
</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: Homo sapiens]] | |||
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
[[Category: | [[Category: Phage display vector pTDisp]] | ||
[[Category: Huang | [[Category: Huang M]] | ||
[[Category: Jiang | [[Category: Jiang L]] | ||
Latest revision as of 10:51, 22 November 2023
Crystal structure of uPA in complex with upain-2-4-W3ACrystal structure of uPA in complex with upain-2-4-W3A
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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