4zkn: Difference between revisions
Jump to navigation
Jump to search
m Protected "4zkn" [edit=sysop:move=sysop] |
No edit summary |
||
| (4 intermediate revisions by the same user not shown) | |||
| Line 1: | Line 1: | ||
The entry | ==The crystal structure of upain-1-W3A in complex with uPA at pH5.5== | ||
<StructureSection load='4zkn' size='340' side='right'caption='[[4zkn]], [[Resolution|resolution]] 1.36Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[4zkn]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Synthetic_construct Synthetic construct]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ZKN OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4ZKN 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]] 1.36Å</td></tr> | |||
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=PG4:TETRAETHYLENE+GLYCOL'>PG4</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=4zkn FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4zkn OCA], [https://pdbe.org/4zkn PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4zkn RCSB], [https://www.ebi.ac.uk/pdbsum/4zkn PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4zkn 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== | |||
*[[Plasminogen activator|Plasminogen activator]] | |||
*[[Urokinase 3D Structures|Urokinase 3D Structures]] | |||
[[Category: | == References == | ||
[[Category: | <references/> | ||
[[Category: | __TOC__ | ||
[[Category: | </StructureSection> | ||
[[Category: Homo sapiens]] | |||
[[Category: Large Structures]] | |||
[[Category: Synthetic construct]] | |||
[[Category: Andreasen PA]] | |||
[[Category: Huang M]] | |||
[[Category: Jiang L]] | |||
Latest revision as of 18:45, 8 November 2023
The crystal structure of upain-1-W3A in complex with uPA at pH5.5The crystal structure of upain-1-W3A in complex with uPA at pH5.5
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
|
| ||||||||||||||||||