4mny: Difference between revisions

Line 1:

~~'''Unreleased~~ structure~~'''~~

===Crystal structure of urokinase-type plasminogen activator (uPA) complexed with bicyclic peptide UK903===

The ~~entry 4mny~~ is ~~ON HOLD~~

==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>

~~Authors~~: ~~Chen, S~~.~~, Pojer, F~~.~~, Heinis, C~~.

==Function==

[[http://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN]] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.

~~Description~~: ~~Crystal structure of urokinase~~-~~type~~ plasminogen activator ~~(uPA) complexed with bicyclic~~ peptide ~~UK903~~

==About this Structure==

[[4mny]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4MNY OCA].

==Reference==

[[Category: U-plasminogen activator]]

[[Category: Chen, S.]]

[[Category: Heinis, C.]]

[[Category: Pojer, F.]]

[[Category: Bicyclic peptide]]

[[Category: Competitive inhibitor]]

[[Category: Extracellular]]

[[Category: Hydrolase-hydrolase inhibitor complex]]

[[Category: Inhibitor]]

[[Category: Ns']]

[[Category: Protease]]

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@@ Line 1: / Line 1: @@
-'''Unreleased structure'''
+{{STRUCTURE_4mny|  PDB=4mny  |  SCENE=  }}
+===Crystal structure of urokinase-type plasminogen activator (uPA) complexed with bicyclic peptide UK903===
+{{ABSTRACT_PUBMED_24453110}}
-The entry 4mny is ON HOLD
+==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>
-Authors: Chen, S., Pojer, F., Heinis, C.
+==Function==
+[[http://www.uniprot.org/uniprot/UROK_HUMAN UROK_HUMAN]] Specifically cleaves the zymogen plasminogen to form the active enzyme plasmin.
-Description: Crystal structure of urokinase-type plasminogen activator (uPA) complexed with bicyclic peptide UK903
+==About this Structure==
+[[4mny]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4MNY 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: Bicyclic peptide]]
+[[Category: Competitive inhibitor]]
+[[Category: Extracellular]]
+[[Category: Hydrolase-hydrolase inhibitor complex]]
+[[Category: Inhibitor]]
+[[Category: Ns']]
+[[Category: Protease]]