5yc7: Difference between revisions
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The entry | ==The crystal structure of uPA in complex with 4-Bromobenzylamirne at pH7.4== | ||
<StructureSection load='5yc7' size='340' side='right' caption='[[5yc7]], [[Resolution|resolution]] 2.00Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[5yc7]] is a 1 chain structure. This structure supersedes the now removed PDB entry [http://oca.weizmann.ac.il/oca-bin/send-pdb?obs=1&id=4jnl 4jnl]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5YC7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5YC7 FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=PZH:1-(4-BROMOPHENYL)METHANAMINE'>PZH</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</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: Huang, M | <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=5yc7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5yc7 OCA], [http://pdbe.org/5yc7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5yc7 RCSB], [http://www.ebi.ac.uk/pdbsum/5yc7 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5yc7 ProSAT]</span></td></tr> | ||
[[Category: Jiang, L | </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: Huang, M D]] | |||
[[Category: Jiang, L G]] | |||
[[Category: Zhang, X]] | [[Category: Zhang, X]] | ||
[[Category: Halogen bonding]] | |||
[[Category: Hydrolase-hydrolase inhibitor complex]] | |||
[[Category: P1 group]] | |||
[[Category: Protease inhibitor]] | |||
[[Category: Serine protease]] | |||
[[Category: Upa]] | |||
Revision as of 10:34, 3 October 2018
The crystal structure of uPA in complex with 4-Bromobenzylamirne at pH7.4The crystal structure of uPA in complex with 4-Bromobenzylamirne 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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