4c26 | pdb_00004c26

NMR structure of the HicA toxin from Burkholderia pseudomallei

spinqualitylabelsall models 4c26, 10 NMR models Show:Asymmetric Unit Biological Assembly Drag the structure with the mouse to rotate   Export Animated Image   Print3D Structural highlights 4c26 is a 1 chain structure with sequence from Burps. Full experimental information is available from OCA. For a guided tour on the structure components use FirstGlance. Resources: FirstGlance, OCA, PDBe, RCSB, PDBsum Publication Abstract from PubMed TA (toxin-antitoxin) systems are widely distributed amongst bacteria and are associated with the formation of antibiotic tolerant (persister) cells that may have involvement in chronic and recurrent disease. We show that overexpression of the Burkholderia pseudomallei HicA toxin causes growth arrest and increases the number of persister cells tolerant to ciprofloxacin or ceftazidime. Furthermore, our data show that persistence towards ciprofloxacin or ceftazidime can be differentially modulated depending on the level of induction of HicA expression. Deleting the hicAB locus from B. pseudomallei K96243 significantly reduced persister cell frequencies following exposure to ciprofloxacin, but not ceftazidime. The structure of HicA(H24A) was solved by NMR and forms a dsRBD-like (dsRNA-binding domain-like) fold, composed of a triple-stranded beta-sheet, with two helices packed against one face. The surface of the protein is highly positively charged indicative of an RNA-binding protein and His24 and Gly22 were functionality important residues. This is the first study demonstrating a role for the HicAB system in bacterial persistence and the first structure of a HicA protein that has been experimentally characterized. The HicA toxin from Burkholderia pseudomallei has a role in persister cell formation.,Butt A, Higman VA, Williams C, Crump MP, Hemsley CM, Harmer N, Titball RW Biochem J. 2014 Apr 15;459(2):333-44. doi: 10.1042/BJ20140073. PMID:24502667 From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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