6ag7: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
No edit summary |
||
| Line 1: | Line 1: | ||
The | ==The crystal structure of uPA in complex with HMA-55F== | ||
<StructureSection load='6ag7' size='340' side='right'caption='[[6ag7]], [[Resolution|resolution]] 1.90Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[6ag7]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6AG7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6AG7 FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=H55:3,5-diamino-N-carbamimidoyl-6-(1-methyl-1H-pyrazol-4-yl)pyrazine-2-carboxamide'>H55</scene></td></tr> | |||
[[Category: | <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> | ||
[[Category: | <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=6ag7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ag7 OCA], [http://pdbe.org/6ag7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6ag7 RCSB], [http://www.ebi.ac.uk/pdbsum/6ag7 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6ag7 ProSAT]</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: Large Structures]] | |||
[[Category: U-plasminogen activator]] | |||
[[Category: Buckley, B]] | |||
[[Category: Huang, M D]] | |||
[[Category: Jiang, L G]] | |||
[[Category: Kelso, M]] | [[Category: Kelso, M]] | ||
[[Category: Majed, H]] | [[Category: Majed, H]] | ||
[[Category: | [[Category: Ranson, M]] | ||
[[Category: | [[Category: Amiloride]] | ||
[[Category: Hydrolase]] | |||
[[Category: Urokinase]] | |||
Revision as of 19:25, 14 August 2019
The crystal structure of uPA in complex with HMA-55FThe crystal structure of uPA in complex with HMA-55F
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
|
| ||||||||||||||||||