4mnx: Difference between revisions
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{{STRUCTURE_4mnx| PDB=4mnx | SCENE= }} | |||
===Crystal structure of urokinase-type plasminogen activator (uPA) complexed with bicyclic peptide UK811=== | |||
{{ABSTRACT_PUBMED_24453110}} | |||
The | ==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> | |||
==Function== | |||
[[http://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN]] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin. | |||
==About this Structure== | |||
[[4mnx]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4MNX OCA]. | |||
==Reference== | |||
<ref group="xtra">PMID:024453110</ref><references group="xtra"/><references/> | |||
[[Category: U-plasminogen activator]] | |||
[[Category: Chen, S.]] | |||
[[Category: Heinis, C.]] | |||
[[Category: Pojer, F.]] | |||
[[Category: 1s']] | |||
[[Category: 5-triazinane-1]] | |||
[[Category: Bicyclic peptide]] | |||
[[Category: Competitive inhibitor]] | |||
[[Category: Extracellular]] | |||
[[Category: Hydrolase-hydrolase inhibitor complex]] | |||
[[Category: Inhibitor]] | |||
[[Category: Protease]] | |||
Revision as of 14:06, 5 February 2014
Crystal structure of urokinase-type plasminogen activator (uPA) complexed with bicyclic peptide UK811Crystal structure of urokinase-type plasminogen activator (uPA) complexed with bicyclic peptide UK811
Template:ABSTRACT PUBMED 24453110
DiseaseDisease
[UROK_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]
FunctionFunction
[UROK_HUMAN] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.
About this StructureAbout this Structure
4mnx is a 2 chain structure. Full crystallographic information is available from OCA.
ReferenceReference
- ↑ Chen S, Bertoldo D, Angelini A, Pojer F, Heinis C. Peptide ligands stabilized by small molecules. Angew Chem Int Ed Engl. 2014 Feb 3;53(6):1602-6. doi: 10.1002/anie.201309459., Epub 2014 Jan 22. PMID:24453110 doi:http://dx.doi.org/10.1002/anie.201309459
- ↑ Paterson AD, Rommens JM, Bharaj B, Blavignac J, Wong I, Diamandis M, Waye JS, Rivard GE, Hayward CP. Persons with Quebec platelet disorder have a tandem duplication of PLAU, the urokinase plasminogen activator gene. Blood. 2010 Feb 11;115(6):1264-6. doi: 10.1182/blood-2009-07-233965. Epub 2009, Dec 9. PMID:20007542 doi:10.1182/blood-2009-07-233965