2nwn
From Proteopedia
(Difference between revisions)
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== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[2nwn]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2NWN OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2NWN FirstGlance]. <br> | <table><tr><td colspan='2'>[[2nwn]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2NWN OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2NWN FirstGlance]. <br> | ||
| - | </td></tr><tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2nwn FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2nwn OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2nwn RCSB], [http://www.ebi.ac.uk/pdbsum/2nwn PDBsum]</span></td></tr> | + | </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=2nwn FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2nwn OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2nwn RCSB], [http://www.ebi.ac.uk/pdbsum/2nwn PDBsum]</span></td></tr> |
| - | <table> | + | </table> |
== Disease == | == 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> | [[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> | ||
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</StructureSection> | </StructureSection> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
| - | [[Category: Andreasen, P A | + | [[Category: Andreasen, P A]] |
| - | [[Category: Huang, M | + | [[Category: Huang, M]] |
| - | [[Category: Huang, Z | + | [[Category: Huang, Z]] |
| - | [[Category: | + | [[Category: Structural genomic]] |
| - | [[Category: Wind, T | + | [[Category: Wind, T]] |
| - | [[Category: Yuan, C | + | [[Category: Yuan, C]] |
| - | [[Category: Zhao, G | + | [[Category: Zhao, G]] |
[[Category: Hydrolase]] | [[Category: Hydrolase]] | ||
[[Category: Peptidyl inhibitor]] | [[Category: Peptidyl inhibitor]] | ||
[[Category: Pharmacophore]] | [[Category: Pharmacophore]] | ||
[[Category: Sgc]] | [[Category: Sgc]] | ||
| - | [[Category: Structural genomic]] | ||
| - | [[Category: Structural genomics consortium]] | ||
[[Category: Urokinase-type plasminogen activator]] | [[Category: Urokinase-type plasminogen activator]] | ||
Revision as of 18:42, 19 January 2015
New Pharmacophore for Serine Protease Inhibition Revealed by Crystal Structure of Human Urokinase-type Plasminogen Activator Complexed with a Cyclic Peptidyl Inhibitor, upain-1
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