4h42: Difference between revisions

From Proteopedia
Jump to navigationJump to search
OCA (talk | contribs)
No edit summary
OCA (talk | contribs)
No edit summary
 
(4 intermediate revisions by the same user not shown)
Line 1: Line 1:
'''Unreleased structure'''


The entry 4h42 is ON HOLD  until Paper Publication
==Synthesis of a Weak Basic uPA Inhibitor and Crystal Structure of Complex with uPA==
<StructureSection load='4h42' size='340' side='right'caption='[[4h42]], [[Resolution|resolution]] 2.01&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[4h42]] 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=4H42 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4H42 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]] 2.01&#8491;</td></tr>
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=11E:N-[(2-AMINO-1,3-BENZOTHIAZOL-6-YL)CARBONYL]GLYCINE'>11E</scene>, <scene name='pdbligand=PG6:1-(2-METHOXY-ETHOXY)-2-{2-[2-(2-METHOXY-ETHOXY]-ETHOXY}-ETHANE'>PG6</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=4h42 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4h42 OCA], [https://pdbe.org/4h42 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4h42 RCSB], [https://www.ebi.ac.uk/pdbsum/4h42 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4h42 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.


Authors: Yu, H.-Y., Gao, D., Zhang, X., Jiang, L.-G., Hong, Z.-B., Yuan, C., Fang, X., Wang, J.-D., Huang, M.-D.
==See Also==
 
*[[Urokinase 3D Structures|Urokinase 3D Structures]]
Description: Synthesis of a Weak Basic uPA Inhibitor and Crystal Structure of Complex with uPA
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Fang X]]
[[Category: Gao D]]
[[Category: Hong Z-B]]
[[Category: Huang M-D]]
[[Category: Jiang L-G]]
[[Category: Wang J-D]]
[[Category: Yu H-Y]]
[[Category: Yuan C]]
[[Category: Zhang X]]