4xsk

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(New page: '''Unreleased structure''' The entry 4xsk is ON HOLD Authors: Lihu Gong, Valerie Proulle, Zebin Hong, Zhonghui Lin, Min Liu, Cai Yuan, Lin Lin, Barbara Furie, Robert Flaumenhaft, Peter ...)
Current revision (15:30, 8 November 2023) (edit) (undo)
 
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'''Unreleased structure'''
 
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The entry 4xsk is ON HOLD
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==Structure of PAItrap, an uPA mutant==
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<StructureSection load='4xsk' size='340' side='right'caption='[[4xsk]], [[Resolution|resolution]] 1.50&Aring;' scene=''>
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== Structural highlights ==
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<table><tr><td colspan='2'>[[4xsk]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4XSK OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4XSK FirstGlance]. <br>
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</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.5&#8491;</td></tr>
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<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=PGE:TRIETHYLENE+GLYCOL'>PGE</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=4xsk FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4xsk OCA], [https://pdbe.org/4xsk PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4xsk RCSB], [https://www.ebi.ac.uk/pdbsum/4xsk PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4xsk ProSAT]</span></td></tr>
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</table>
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== Disease ==
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[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>
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== Function ==
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[https://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.
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Authors: Lihu Gong, Valerie Proulle, Zebin Hong, Zhonghui Lin, Min Liu, Cai Yuan, Lin Lin, Barbara Furie, Robert Flaumenhaft, Peter Andreasen, Bruce Furie, Mingdong Huang
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==See Also==
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*[[Plasminogen activator|Plasminogen activator]]
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Description: PAItrap, an uPA mutant
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*[[Urokinase 3D Structures|Urokinase 3D Structures]]
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[[Category: Unreleased Structures]]
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== References ==
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[[Category: Lihu Gong, Valerie Proulle, Zebin Hong, Zhonghui Lin, Min Liu, Cai Yuan, Lin Lin, Barbara Furie, Robert Flaumenhaft, Peter Andreasen, Bruce Furie, Mingdong Huang]]
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<references/>
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__TOC__
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</StructureSection>
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[[Category: Homo sapiens]]
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[[Category: Large Structures]]
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[[Category: Andreasen P]]
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[[Category: Flaumenhaft R]]
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[[Category: Furie B]]
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[[Category: Gong L]]
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[[Category: Hong Z]]
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[[Category: Huang M]]
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[[Category: Lin L]]
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[[Category: Lin Z]]
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[[Category: Liu M]]
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[[Category: Proulle V]]
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[[Category: Yuan C]]

Current revision

Structure of PAItrap, an uPA mutant

PDB ID 4xsk

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