Pages that link to "Q28548282"
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The following pages link to Mycobacterium tuberculosis Is Resistant to Isoniazid at a Slow Growth Rate by Single Nucleotide Polymorphisms in katG Codon Ser315 (Q28548282):
Displaying 13 items.
- Isoniazid-resistant tuberculosis: a cause for concern? (Q33820505) (← links)
- The effect of growth rate on pyrazinamide activity in Mycobacterium tuberculosis - insights for early bactericidal activity? (Q36019139) (← links)
- A Flow Cytometry Method for Rapidly Assessing Mycobacterium tuberculosis Responses to Antibiotics with Different Modes of Action (Q37023216) (← links)
- Diverse drug-resistant subpopulations of Mycobacterium tuberculosis are sustained in continuous culture (Q37466064) (← links)
- Roles of Regulatory RNAs for Antibiotic Resistance in Bacteria and Their Potential Value as Novel Drug Targets (Q39321244) (← links)
- Isoniazid Killing of Mycobacterium smegmatis NADH Pyrophosphatase Mutant at Single-Cell Level using Microfluidics and Time-Lapse Microscopy (Q41543191) (← links)
- Potential and use of bacterial small RNAs to combat drug resistance: a systematic review. (Q47096824) (← links)
- Mutations in catalase-peroxidase KatG from isoniazid resistant Mycobacterium tuberculosis clinical isolates: insights from molecular dynamics simulations. (Q48112845) (← links)
- Application of Continuous Culture for Assessing Antibiotic Activity Against Mycobacterium tuberculosis (Q50097373) (← links)
- A comparison of Rv0559c and Rv0560c expression in drug-resistant Mycobacterium tuberculosis in response to first-line antituberculosis drugs. (Q52663859) (← links)
- Altered Mycobacterium tuberculosis Cell Wall Metabolism and Physiology Associated With RpoB Mutation H526D. (Q53698585) (← links)
- Efflux Pumps in Mycobacteria: Antimicrobial Resistance, Physiological Functions, and Role in Pathogenicity (Q57656351) (← links)
- Re-growth of Mycobacterium tuberculosis populations exposed to antibiotic combinations is due to the presence of isoniazid and not bacterial growth rate (Q90131019) (← links)