4zn2

</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=4zn2 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4zn2 OCA], [https://pdbe.org/4zn2 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4zn2 RCSB], [https://www.ebi.ac.uk/pdbsum/4zn2 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4zn2 ProSAT]</span></td></tr>

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== Publication Abstract from PubMed ==

Biofilms are surface-associated communities of microorganism embedded in extracellular matrix. Exopolysaccharide is a critical component in the extracellular matrix that maintains biofilm architecture and protects resident biofilm bacteria from antimicrobials and host immune attack. However, self-produced factors that target the matrix exopolysaccharides, are still poorly understood. Here, we show that PslG, a protein involved in the synthesis of a key biofilm matrix exopolysaccharide Psl in Pseudomonas aeruginosa, prevents biofilm formation and disassembles existing biofilms within minutes at nanomolar concentrations when supplied exogenously. The crystal structure of PslG indicates the typical features of an endoglycosidase. PslG mainly disrupts the Psl matrix to disperse bacteria from biofilms. PslG treatment markedly enhances biofilm sensitivity to antibiotics and macrophage cells, resulting in improved biofilm clearance in a mouse implant infection model. Furthermore, PslG shows biofilm inhibition and disassembly activity against a wide range of Pseudomonas species, indicating its great potential in combating biofilm-related complications.

PslG, a self-produced glycosyl hydrolase, triggers biofilm disassembly by disrupting exopolysaccharide matrix.,Yu S, Su T, Wu H, Liu S, Wang D, Zhao T, Jin Z, Du W, Zhu MJ, Chua SL, Yang L, Zhu D, Gu L, Ma LZ Cell Res. 2015 Dec;25(12):1352-67. doi: 10.1038/cr.2015.129. Epub 2015 Nov 27. PMID:26611635<ref>PMID:26611635</ref>

From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>

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== References ==

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