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The | ==The crystal structure of upain-1-W3A in complex with uPA at pH7.4== | ||
<StructureSection load='4zko' size='340' side='right' caption='[[4zko]], [[Resolution|resolution]] 1.29Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[4zko]] is a 3 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ZKO OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4ZKO FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=P6G:HEXAETHYLENE+GLYCOL'>P6G</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr> | |||
[[Category: | <tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[4zkn|4zkn]], [[4zkr|4zkr]], [[4zks|4zks]]</td></tr> | ||
<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> | |||
<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=4zko FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4zko OCA], [http://pdbe.org/4zko PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4zko RCSB], [http://www.ebi.ac.uk/pdbsum/4zko PDBsum]</span></td></tr> | |||
</table> | |||
== Disease == | |||
[[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> | |||
== Function == | |||
[[http://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN]] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin. | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: U-plasminogen activator]] | |||
[[Category: Andreasen, P A]] | |||
[[Category: Huang, M]] | [[Category: Huang, M]] | ||
[[Category: Jiang, L]] | [[Category: Jiang, L]] | ||
[[Category: | [[Category: Hydrolase-hydrolase inhibitor complex]] | ||
[[Category: Peptides inhibitor]] | |||
[[Category: Serine protease]] | |||
[[Category: Upa]] | |||
Revision as of 18:47, 1 June 2016
The crystal structure of upain-1-W3A in complex with uPA at pH7.4The crystal structure of upain-1-W3A in complex with uPA at pH7.4
Structural highlights
Disease[UROK_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] Function[UROK_HUMAN] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin. References
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