View source for 4dmk


==Crystal structure of the CFTR inhibitory factor Cif with the Y239F mutation==
<StructureSection load='4dmk' size='340' side='right' caption='[[4dmk]], [[Resolution|resolution]] 1.50&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[4dmk]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Pseab Pseab]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4DMK OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4DMK FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[3kd2|3kd2]], [[3kda|3kda]], [[3pi6|3pi6]], [[4dln|4dln]], [[4dm7|4dm7]], [[4dmc|4dmc]], [[4dmf|4dmf]], [[4dmh|4dmh]], [[4dnf|4dnf]], [[4dno|4dno]]</td></tr>
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">PA14_26090 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=208963 PSEAB])</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=4dmk FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4dmk OCA], [http://pdbe.org/4dmk PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4dmk RCSB], [http://www.ebi.ac.uk/pdbsum/4dmk PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4dmk ProSAT]</span></td></tr>
</table>
<div style="background-color:#fffaf0;">
== Publication Abstract from PubMed ==
Opportunistic pathogens exploit diverse strategies to sabotage host defenses. Pseudomonas aeruginosa secretes the CFTR inhibitory factor Cif and thus triggers loss of CFTR, an ion channel required for airway mucociliary defense. However, the mechanism of action of Cif has remained unclear. It catalyzes epoxide hydrolysis, but there is no known role for natural epoxides in CFTR regulation. It was demonstrated that the hydrolase activity of Cif is strictly required for its effects on CFTR. A small-molecule inhibitor that protects this key component of the mucociliary defense system was also uncovered. These results provide a basis for targeting the distinctive virulence chemistry of Cif and suggest an unanticipated role of physiological epoxides in intracellular protein trafficking.

Inhibiting an epoxide hydrolase virulence factor from Pseudomonas aeruginosa protects CFTR.,Bahl CD, Hvorecny KL, Bomberger JM, Stanton BA, Hammock BD, Morisseau C, Madden DR Angew Chem Int Ed Engl. 2015 Jul 1. doi: 10.1002/anie.201503983. PMID:26136396<ref>PMID:26136396</ref>

From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
</div>
<div class="pdbe-citations 4dmk" style="background-color:#fffaf0;"></div>
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Pseab]]
[[Category: Bahl, C D]]
[[Category: Madden, D R]]
[[Category: Alpha beta hydrolase]]
[[Category: Epoxide hydrolase]]
[[Category: Hydrolase]]
[[Category: Secreted]]