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{{STRUCTURE_2viw| PDB=2viw | SCENE= }} | {{STRUCTURE_2viw| PDB=2viw | SCENE= }} | ||
===FRAGMENT-BASED DISCOVERY OF MEXILETINE DERIVATIVES AS ORALLY BIOAVAILABLE INHIBITORS OF UROKINASE-TYPE PLASMINOGEN ACTIVATOR=== | |||
{{ABSTRACT_PUBMED_18163548}} | |||
=== | ==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== | ==About this Structure== | ||
| Line 14: | Line 16: | ||
==Reference== | ==Reference== | ||
<ref group="xtra">PMID:018163548</ref><references group="xtra"/> | <ref group="xtra">PMID:018163548</ref><references group="xtra"/><references/> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: U-plasminogen activator]] | [[Category: U-plasminogen activator]] | ||
Revision as of 04:16, 25 March 2013
FRAGMENT-BASED DISCOVERY OF MEXILETINE DERIVATIVES AS ORALLY BIOAVAILABLE INHIBITORS OF UROKINASE-TYPE PLASMINOGEN ACTIVATORFRAGMENT-BASED DISCOVERY OF MEXILETINE DERIVATIVES AS ORALLY BIOAVAILABLE INHIBITORS OF UROKINASE-TYPE PLASMINOGEN ACTIVATOR
Template:ABSTRACT PUBMED 18163548
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
2viw is a 1 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA.
See AlsoSee Also
ReferenceReference
- ↑ Frederickson M, Callaghan O, Chessari G, Congreve M, Cowan SR, Matthews JE, McMenamin R, Smith DM, Vinkovic M, Wallis NG. Fragment-based discovery of mexiletine derivatives as orally bioavailable inhibitors of urokinase-type plasminogen activator. J Med Chem. 2008 Jan 24;51(2):183-6. Epub 2007 Dec 29. PMID:18163548 doi:http://dx.doi.org/10.1021/jm701359z
- ↑ 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
Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)
OCACategories:
- Homo sapiens
- U-plasminogen activator
- Callaghan, O.
- Chessari, G.
- Congreve, M.
- Cowan, S R.
- Frederickson, M.
- Matthews, J E.
- Mcmenamin, R.
- Smith, D.
- Vinkovic, M.
- Wallis, N G.
- Blood coagulation
- Egf-like domain
- Fibrinolysis
- Glycoprotein
- Hydrolase
- Inhibitor
- Kringle
- Phosphorylation
- Plasminogen activation
- Protease
- Secreted
- Serine protease
- Urokinase-type plasminogen activator
- Zymogen