4x0w: Difference between revisions

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<StructureSection load='4x0w' size='340' side='right'caption='[[4x0w]], [[Resolution|resolution]] 2.10&Aring;' scene=''>
<StructureSection load='4x0w' size='340' side='right'caption='[[4x0w]], [[Resolution|resolution]] 2.10&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[4x0w]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4X0W OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4X0W FirstGlance]. <br>
<table><tr><td colspan='2'>[[4x0w]] 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=4X0W OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4X0W FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=MRZ:PIPERIDINE-1-CARBOXIMIDAMIDE'>MRZ</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=DAL:D-ALANINE'>DAL</scene>, <scene name='pdbligand=MRZ:PIPERIDINE-1-CARBOXIMIDAMIDE'>MRZ</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=DAL:D-ALANINE'>DAL</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=4x0w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4x0w OCA], [https://pdbe.org/4x0w PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4x0w RCSB], [https://www.ebi.ac.uk/pdbsum/4x0w PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4x0w ProSAT]</span></td></tr>
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[4x1n|4x1n]], [[4n1p|4n1p]], [[4n1q|4n1q]], [[4n1r|4n1r]], [[4n1s|4n1s]]</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=4x0w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4x0w OCA], [http://pdbe.org/4x0w PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4x0w RCSB], [http://www.ebi.ac.uk/pdbsum/4x0w PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4x0w ProSAT]</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>
[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 ==
== Function ==
[[http://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN]] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.  
[https://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.
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<div style="background-color:#fffaf0;">
== Publication Abstract from PubMed ==
== Publication Abstract from PubMed ==
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==See Also==
==See Also==
*[[Plasminogen activator|Plasminogen activator]]
*[[Plasminogen activator|Plasminogen activator]]
*[[Urokinase|Urokinase]]
*[[Urokinase 3D Structures|Urokinase 3D Structures]]
== References ==
== References ==
<references/>
<references/>
__TOC__
__TOC__
</StructureSection>
</StructureSection>
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Large Structures]]
[[Category: U-plasminogen activator]]
[[Category: Synthetic construct]]
[[Category: Andreasen, P]]
[[Category: Andreasen P]]
[[Category: Huang, M]]
[[Category: Huang M]]
[[Category: Jiang, L]]
[[Category: Jiang L]]
[[Category: Xu, P]]
[[Category: Xu P]]
[[Category: Zhao, B]]
[[Category: Zhao B]]
[[Category: Hydrolase inhibitor-hydrolase complex]]
[[Category: Hydrolase-hydrolase inhibitor complex]]
[[Category: Peptidic inhibitor]]
[[Category: Serine protease]]

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