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The | ==Crystal structure of uPA in complex with 3,5-bis(azanyl)-6-(1-benzofuran-2-yl)-N-carbamimidoyl-pyrazine-2- carboxamide== | ||
<StructureSection load='6ag9' size='340' side='right'caption='[[6ag9]], [[Resolution|resolution]] 1.63Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[6ag9]] 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=6AG9 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6AG9 FirstGlance]. <br> | |||
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.63Å</td></tr> | |||
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=9XF:3,5-bis(azanyl)-6-(1-benzofuran-2-yl)-N-carbamimidoyl-pyrazine-2-carboxamide'>9XF</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=6ag9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ag9 OCA], [https://pdbe.org/6ag9 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6ag9 RCSB], [https://www.ebi.ac.uk/pdbsum/6ag9 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6ag9 ProSAT]</span></td></tr> | |||
</table> | |||
== 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 == | |||
[https://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin. | |||
==See Also== | |||
*[[Urokinase 3D Structures|Urokinase 3D Structures]] | |||
== References == | |||
[[Category: | <references/> | ||
[[Category: | __TOC__ | ||
[[Category: | </StructureSection> | ||
[[Category: | [[Category: Homo sapiens]] | ||
[[Category: | [[Category: Large Structures]] | ||
[[Category: | [[Category: Buckley B]] | ||
[[Category: | [[Category: Huang MD]] | ||
[[Category: Jiang LG]] | |||
[[Category: Kelso M]] | |||
[[Category: Majed H]] | |||
[[Category: Ranson M]] | |||
Revision as of 12:30, 22 November 2023
Crystal structure of uPA in complex with 3,5-bis(azanyl)-6-(1-benzofuran-2-yl)-N-carbamimidoyl-pyrazine-2- carboxamideCrystal structure of uPA in complex with 3,5-bis(azanyl)-6-(1-benzofuran-2-yl)-N-carbamimidoyl-pyrazine-2- carboxamide
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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