3ut3: Difference between revisions

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[[Image:3ut3.jpg|left|200px]]
==A novel PAI-I inhibitor and its structural mechanism==
<StructureSection load='3ut3' size='340' side='right' caption='[[3ut3]], [[Resolution|resolution]] 2.42&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[3ut3]] is a 4 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=3UT3 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3UT3 FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EMJ:2,5-DIHYDROXY-3-UNDECYLCYCLOHEXA-2,5-DIENE-1,4-DIONE'>EMJ</scene></td></tr>
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">SERPINE1, PAI1, PLANH1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3ut3 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3ut3 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3ut3 RCSB], [http://www.ebi.ac.uk/pdbsum/3ut3 PDBsum]</span></td></tr>
</table>
== Disease ==
[[http://www.uniprot.org/uniprot/PAI1_HUMAN PAI1_HUMAN]] Defects in SERPINE1 are the cause of plasminogen activator inhibitor-1 deficiency (PAI-1D) [MIM:[http://omim.org/entry/613329 613329]]. It is a hematologic disorder characterized by increased bleeding after trauma, injury, or surgery. Affected females have menorrhagia. The bleeding defect is due to increased fibrinolysis of fibrin blood clots due to deficiency of plasminogen activator inhibitor-1, which inhibits tissue and urinary activators of plasminogen.<ref>PMID:9207454</ref>  Note=High concentrations of SERPINE1 seem to contribute to the development of venous but not arterial occlusions.
== Function ==
[[http://www.uniprot.org/uniprot/PAI1_HUMAN PAI1_HUMAN]] Serine protease inhibitor. This inhibitor acts as 'bait' for tissue plasminogen activator, urokinase, protein C and matriptase-3/TMPRSS7. Its rapid interaction with PLAT may function as a major control point in the regulation of fibrinolysis.<ref>PMID:15853774</ref> 


{{STRUCTURE_3ut3|  PDB=3ut3  |  SCENE= }}
==See Also==
 
*[[Plasminogen activator inhibitor|Plasminogen activator inhibitor]]
===A novel PAI-I inhibitor and its structural mechanism===
== References ==
 
<references/>
 
__TOC__
==About this Structure==
</StructureSection>
[[3ut3]] is a 4 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=3UT3 OCA].
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Andreasen, P A.]]
[[Category: Andreasen, P A]]
[[Category: Hong, Z B.]]
[[Category: Hong, Z B]]
[[Category: Hu, L H.]]
[[Category: Hu, L H]]
[[Category: Huang, M D.]]
[[Category: Huang, M D]]
[[Category: Lin, Z H.]]
[[Category: Lin, Z H]]
[[Category: Shi, X L.]]
[[Category: Shi, X L]]
[[Category: Hydrolase inhibitor]]
[[Category: Hydrolase inhibitor]]
[[Category: Serpin]]
[[Category: Serpin]]

Revision as of 11:53, 25 December 2014

A novel PAI-I inhibitor and its structural mechanismA novel PAI-I inhibitor and its structural mechanism

Structural highlights

3ut3 is a 4 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA. For a guided tour on the structure components use FirstGlance.
Ligands:
Gene:SERPINE1, PAI1, PLANH1 (Homo sapiens)
Resources:FirstGlance, OCA, RCSB, PDBsum

Disease

[PAI1_HUMAN] Defects in SERPINE1 are the cause of plasminogen activator inhibitor-1 deficiency (PAI-1D) [MIM:613329]. It is a hematologic disorder characterized by increased bleeding after trauma, injury, or surgery. Affected females have menorrhagia. The bleeding defect is due to increased fibrinolysis of fibrin blood clots due to deficiency of plasminogen activator inhibitor-1, which inhibits tissue and urinary activators of plasminogen.[1] Note=High concentrations of SERPINE1 seem to contribute to the development of venous but not arterial occlusions.

Function

[PAI1_HUMAN] Serine protease inhibitor. This inhibitor acts as 'bait' for tissue plasminogen activator, urokinase, protein C and matriptase-3/TMPRSS7. Its rapid interaction with PLAT may function as a major control point in the regulation of fibrinolysis.[2]

See Also

References

  1. ↑ Fay WP, Parker AC, Condrey LR, Shapiro AD. Human plasminogen activator inhibitor-1 (PAI-1) deficiency: characterization of a large kindred with a null mutation in the PAI-1 gene. Blood. 1997 Jul 1;90(1):204-8. PMID:9207454
  2. ↑ Szabo R, Netzel-Arnett S, Hobson JP, Antalis TM, Bugge TH. Matriptase-3 is a novel phylogenetically preserved membrane-anchored serine protease with broad serpin reactivity. Biochem J. 2005 Aug 15;390(Pt 1):231-42. PMID:15853774 doi:BJ20050299

3ut3, resolution 2.42Å

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