5n1c
From Proteopedia
(Difference between revisions)
m (Protected "5n1c" [edit=sysop:move=sysop]) |
|||
| Line 1: | Line 1: | ||
| - | '''Unreleased structure''' | ||
| - | + | ==Iodinated form of the Mycobacterium tuberculosis repressor EthR2== | |
| + | <StructureSection load='5n1c' size='340' side='right' caption='[[5n1c]], [[Resolution|resolution]] 2.60Å' scene=''> | ||
| + | == Structural highlights == | ||
| + | <table><tr><td colspan='2'>[[5n1c]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5N1C OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5N1C FirstGlance]. <br> | ||
| + | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=IOD:IODIDE+ION'>IOD</scene></td></tr> | ||
| + | <tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=TYI:3,5-DIIODOTYROSINE'>TYI</scene></td></tr> | ||
| + | <tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[5icj|5icj]]</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=5n1c FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5n1c OCA], [http://pdbe.org/5n1c PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5n1c RCSB], [http://www.ebi.ac.uk/pdbsum/5n1c PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5n1c ProSAT]</span></td></tr> | ||
| + | </table> | ||
| + | <div style="background-color:#fffaf0;"> | ||
| + | == Publication Abstract from PubMed == | ||
| + | Antibiotic resistance is one of the biggest threats to human health globally. Alarmingly, multidrug-resistant and extensively drug-resistant Mycobacterium tuberculosis have now spread worldwide. Some key antituberculosis antibiotics are prodrugs, for which resistance mechanisms are mainly driven by mutations in the bacterial enzymatic pathway required for their bioactivation. We have developed drug-like molecules that activate a cryptic alternative bioactivation pathway of ethionamide in M. tuberculosis, circumventing the classic activation pathway in which resistance mutations have now been observed. The first-of-its-kind molecule, named SMARt-420 (Small Molecule Aborting Resistance), not only fully reverses ethionamide-acquired resistance and clears ethionamide-resistant infection in mice, it also increases the basal sensitivity of bacteria to ethionamide. | ||
| - | + | Reversion of antibiotic resistance in Mycobacterium tuberculosis by spiroisoxazoline SMARt-420.,Blondiaux N, Moune M, Desroses M, Frita R, Flipo M, Mathys V, Soetaert K, Kiass M, Delorme V, Djaout K, Trebosc V, Kemmer C, Wintjens R, Wohlkonig A, Antoine R, Huot L, Hot D, Coscolla M, Feldmann J, Gagneux S, Locht C, Brodin P, Gitzinger M, Deprez B, Willand N, Baulard AR Science. 2017 Mar 17;355(6330):1206-1211. doi: 10.1126/science.aag1006. Epub 2017, Mar 16. PMID:28302858<ref>PMID:28302858</ref> | |
| - | + | From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | |
| - | + | </div> | |
| + | <div class="pdbe-citations 5n1c" style="background-color:#fffaf0;"></div> | ||
| + | == References == | ||
| + | <references/> | ||
| + | __TOC__ | ||
| + | </StructureSection> | ||
[[Category: Wintjens, R]] | [[Category: Wintjens, R]] | ||
[[Category: Wohlkonig, A]] | [[Category: Wohlkonig, A]] | ||
| + | [[Category: Chemical modification]] | ||
| + | [[Category: Dna binding protein]] | ||
| + | [[Category: Ethr]] | ||
| + | [[Category: Iodination]] | ||
| + | [[Category: Repressor]] | ||
Revision as of 13:50, 27 April 2017
Iodinated form of the Mycobacterium tuberculosis repressor EthR2
| |||||||||||
