4h42

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'''Unreleased structure'''
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{{STRUCTURE_4h42| PDB=4h42 | SCENE= }}
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===Synthesis of a Weak Basic uPA Inhibitor and Crystal Structure of Complex with uPA===
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The entry 4h42 is ON HOLD until Paper Publication
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==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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Authors: Yu, H.-Y., Gao, D., Zhang, X., Jiang, L.-G., Hong, Z.-B., Yuan, C., Fang, X., Wang, J.-D., Huang, M.-D.
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==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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Description: Synthesis of a Weak Basic uPA Inhibitor and Crystal Structure of Complex with uPA
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==About this Structure==
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[[4h42]] is a 1 chain structure with sequence from [http://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].
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==Reference==
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<references group="xtra"/><references/>
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[[Category: Homo sapiens]]
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[[Category: U-plasminogen activator]]
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[[Category: Fang, X.]]
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[[Category: Gao, D.]]
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[[Category: Hong, Z B.]]
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[[Category: Huang, M D.]]
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[[Category: Jiang, L G.]]
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[[Category: Wang, J D.]]
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[[Category: Yu, H Y.]]
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[[Category: Yuan, C.]]
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[[Category: Zhang, X.]]
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[[Category: Hydrolase]]
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[[Category: Hydrolase-inhibitor complex]]
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[[Category: Plasminogen activation]]
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[[Category: Protease]]
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[[Category: Serine protease]]

Revision as of 09:48, 30 October 2013

Template:STRUCTURE 4h42

Contents

Synthesis of a Weak Basic uPA Inhibitor and Crystal Structure of Complex with uPA

Disease

[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]

Function

[UROK_HUMAN] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.

About this Structure

4h42 is a 1 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA.

Reference

  1. ↑ 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

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OCA

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