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6nmb

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Current revision (06:56, 11 October 2023) (edit) (undo)
 
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<StructureSection load='6nmb' size='340' side='right'caption='[[6nmb]], [[Resolution|resolution]] 2.30&Aring;' scene=''>
<StructureSection load='6nmb' size='340' side='right'caption='[[6nmb]], [[Resolution|resolution]] 2.30&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
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<table><tr><td colspan='2'>[[6nmb]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6NMB OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6NMB FirstGlance]. <br>
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<table><tr><td colspan='2'>[[6nmb]] is a 4 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=6NMB OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6NMB FirstGlance]. <br>
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</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=AMH:TRANS-4-AMINOMETHYLCYCLOHEXANE-1-CARBOXYLIC+ACID'>AMH</scene>, <scene name='pdbligand=NO3:NITRATE+ION'>NO3</scene></td></tr>
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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]] 2.3&#8491;</td></tr>
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<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">PLAU ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=AMH:TRANS-4-AMINOMETHYLCYCLOHEXANE-1-CARBOXYLIC+ACID'>AMH</scene>, <scene name='pdbligand=NO3:NITRATE+ION'>NO3</scene></td></tr>
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<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>
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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=6nmb FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6nmb OCA], [https://pdbe.org/6nmb PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6nmb RCSB], [https://www.ebi.ac.uk/pdbsum/6nmb PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6nmb ProSAT]</span></td></tr>
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<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=6nmb FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6nmb OCA], [http://pdbe.org/6nmb PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6nmb RCSB], [http://www.ebi.ac.uk/pdbsum/6nmb PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6nmb ProSAT]</span></td></tr>
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</table>
</table>
== Disease ==
== Disease ==
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[[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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[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 ==
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[[http://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN]] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.
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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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<div style="background-color:#fffaf0;">
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== Publication Abstract from PubMed ==
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TXA is an active-site inhibitor of uPA. TXA attenuates MDA-MB-231 BAG cell migration and inhibits endogenous uPA activity.
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Tranexamic acid is an active site inhibitor of urokinase plasminogen activator.,Wu G, Mazzitelli BA, Quek AJ, Veldman MJ, Conroy PJ, Caradoc-Davies TT, Ooms LM, Tuck KL, Schoenecker JG, Whisstock JC, Law RHP Blood Adv. 2019 Mar 12;3(5):729-733. doi: 10.1182/bloodadvances.2018025429. PMID:30814058<ref>PMID:30814058</ref>
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From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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</div>
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<div class="pdbe-citations 6nmb" style="background-color:#fffaf0;"></div>
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==See Also==
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*[[Urokinase 3D Structures|Urokinase 3D Structures]]
== References ==
== References ==
<references/>
<references/>
__TOC__
__TOC__
</StructureSection>
</StructureSection>
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[[Category: Human]]
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[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Large Structures]]
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[[Category: U-plasminogen activator]]
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[[Category: Law RHP]]
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[[Category: Law, R H.P]]
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[[Category: Wu G]]
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[[Category: Wu, G]]
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[[Category: Fibrinolysis]]
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[[Category: Hydrolase]]
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[[Category: Inhibitor]]
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[[Category: Serine protease]]
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Current revision

Tranexamic Acid is an Active Site Inhibitor of Urokinase Plasminogen Activator

PDB ID 6nmb

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