2013
DOI: 10.1016/j.jprot.2013.08.025
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Proteomic analysis of Mycobacterium tuberculosis isolates resistant to kanamycin and amikacin

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Cited by 68 publications
(67 citation statements)
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“…ACCEPTED MANUSCRIPT 4 the cell [3]. However, exact mechanisms of resistance to FQs are not fully known.…”
Section: Accepted Manuscriptmentioning
confidence: 99%
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“…ACCEPTED MANUSCRIPT 4 the cell [3]. However, exact mechanisms of resistance to FQs are not fully known.…”
Section: Accepted Manuscriptmentioning
confidence: 99%
“…Two-dimensional gel electrophoresis (2-DE) coupled with MALDI-TOF mass spectrometry (MS) and bioinformatics is a powerful and efficient tool for rapid identification of proteins. Comparative proteomic studies addressing whole cell proteins with first and second line drugs resistant isolates have been reported [4][5]. In spite of advancement in mycobacterial research, the knowledge about genes and their corresponding functional proteins under drug pressure with susceptible and resistant isolates with FQs has remained unaddressed.…”
Section: Accepted Manuscriptmentioning
confidence: 99%
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“…In a complementary approach, systems-level analyses have been increasingly applied to investigate mycobacterial mechanisms of resistance to anti-TB drugs (Kumar et al 2013), as well as to elucidate the effect of common drugresistance mutations on bacillary physiology and cell function and, by implication, pathogenesis (Bisson et al 2012;du Preez and Loots 2012;Loots 2014). For example, proteomic profiling of M. tuberculosis isolates resistant to kanamycin and amikacin implicated putative iron homeostatic proteins as well as proteins of unknown function in the metabolic adaptation of mutants resistant to the major second-line aminoglycosides (Kumar et al 2013).…”
Section: The Metabolic Response To Drug Treatmentmentioning
confidence: 99%
“…For example, proteomic profiling of M. tuberculosis isolates resistant to kanamycin and amikacin implicated putative iron homeostatic proteins as well as proteins of unknown function in the metabolic adaptation of mutants resistant to the major second-line aminoglycosides (Kumar et al 2013). Moreover, comparative proteomics of clinical rifampicinresistant isolates has revealed differences in the expression profiles of specific rpoB mutants of the Mtb Haarlem and Beijing lineages compared with corresponding drug-susceptible counterparts (Bisson et al 2012).…”
Section: The Metabolic Response To Drug Treatmentmentioning
confidence: 99%