J Clin Microbiol 2001, 39:2531–40.CrossRefPubMed 38. Hwang H, Chang C, Chang L, Chang S, Chang Y, Chen Y: Characterisation of rifampicin-resistant Mycobacterium tuberculosis in Taiwan. J Clin Microbiol 2003, 52:239–45. 39. Somoskovi
A, Dormandy J, Mitsani D, Rivenburg J, Salfinger M: Use of smear-positive samples to assess the PCR-based genotype MTBDR assay for rapid, direct detection of the Mycobacterium tuberculosis complex as well as its resistance to isoniazid and rifampin. J Clin Microbiol 2006, 44:4459–63.CrossRefPubMed 40. Banerjee A, Dubnau E, Quemard A, Balasubramanian V, Um KS, Wilson T, Cillins D, de Lisle G, Jacobs WR Jr:inhA , a gene encoding a target for isoniazid and ethionamide in Mycobacterium tuberculosis. Science 1994, 263:227–30.CrossRefPubMed learn more 41. Musser JM, Kapur V, Williams DL, Kreiswirth BN, van Soolingen D, van Embden JD: Characterization of the catalase-peroxidase gene ( katG
) and inhA locus in isoniazid-resistant and -susceptible strains of Mycobacterium tuberculosis by automated DNA sequencing: restricted array of mutations associated with drug resistance. J Infect Dis 1996, 173:196–202.PubMed 42. Basso LA, Zheng R, Musser JM, Jacobs WR Jr, Blanchard JS: Mechanisms of isoniazid resistance in Mycobacterium this website tuberculosis : enzymatic characterization of enoyl reductase mutants identified in isoniazid-resistant clinical isolates. J Infect Dis 1998, 178:769–75.CrossRefPubMed 43. Fu LM, Fu-Liu CS: The gene expression data of Mycobacterium tuberculosis based on Affymetrix gene chips provide insight into regulatory and hypothetical genes. BMC Microbiol 2007, 14:7–37. 44. Karakousis PC, Yoshimatsu T, Lamichhane G, Woolwine SC, Nuermberger EL, Grosset J, Bishai WR: Dormancy phenotype displayed by extracellular Mycobacterium tuberculosis within artificial granulomas in mice. J Exp Med 2004, 200:647–57.CrossRefPubMed MYO10 45. Korycka-Machała M, Rumijowska-Galewicz A, Dziadek J: The effect of ethambutol on mycobacterial cell wall permeability to hydrophobic compounds. Pol J Microbiol 2005, 54:5–11.PubMed
Authors’ contributions AZ performed the majority of experiments. AB helped in cloning. EAK and ZZ supervised susceptibility tests. JD conceived and supervised the study and wrote the manuscript. All authors have read and approved the final version of the manuscript.”
“Background Knowledge of the different proteins and cellular processes affected by chemicals is necessary to rationally guide drug discovery and development. This is a MX69 price difficult challenge because unbiased techniques to sample all possible target proteins and pathways are currently lacking. The observation that modifying the amount or activity of a gene product via mutation, overexpression, downregulation or deletion can change the response of a cell to a chemical [1, 2] raises hope that systematic genome-wide screens of drug sensitivity can help uncover direct and indirect drug targets as well as modifiers of cellular responses to chemicals.