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katG  -  catalase-peroxidase

Mycobacterium tuberculosis CDC1551

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Disease relevance of katG


High impact information on katG


Chemical compound and disease context of katG


Biological context of katG


Anatomical context of katG


Associations of katG with chemical compounds

  • Sequencing of consecutive isolates identified by the National Tuberculosis Program showed 89% of isoniazid-resistant isolates could be detected by targeting just 2 codons, katG 315 and -15C-->T in the inhA promoter, while rifampin resistance will be more complex to detect, with many different mutation and insertion events in rpoB [22].
  • Isoniazid is a pro-drug, which, after activation by the katG-encoded catalase peroxidase, reacts nonenzymatically with NAD(+) and NADP(+) to generate several isonicotinoyl adducts of these pyridine nucleotides [23].
  • Mutations in katG, ahpC, and inhA were associated with rifampin resistance, but only katG315 mutations were associated with ethambutol resistance [24].
  • This promoter mutation occurred alone without katG mutations and was associated with a low level of INH and ethionamide resistance [25].
  • Resistance may be mediated by mycobacterial catalase-peroxidase (KatG) and possibly by alkyl hydroperoxide reductase (AhpC) [26].

Other interactions of katG

  • The Genotype MTBDR assay is designed to detect mutations within the 81-bp hotspot region of rpoB and mutations at katG codon 315 [16].
  • The strains present in the mummified remains were identified as M. tuberculosis and not Mycobacterium bovis, from katG and gyrA genotyping, PCR from the oxyR and mtp40 loci, and spoligotyping [27].
  • Surprisingly, most INH-resistant strains with KatG codon 315 substitutions that substantially reduce catalase-peroxidase activity and confer high MICs of INH lacked alterations in the ahpC gene or oxyR-ahpC intervening region [28].

Analytical, diagnostic and therapeutic context of katG


  1. Association between Mycobacterium tuberculosis Beijing/W Lineage Strain Infection and Extrathoracic Tuberculosis: Insights from Epidemiologic and Clinical Characterization of the Three Principal Genetic Groups of M. tuberculosis Clinical Isolates. Kong, Y., Cave, M.D., Zhang, L., Foxman, B., Marrs, C.F., Bates, J.H., Yang, Z.H. J. Clin. Microbiol. (2007) [Pubmed]
  2. Detection of Multidrug Resistance in Mycobacterium tuberculosis. Sekiguchi, J., Miyoshi-Akiyama, T., Augustynowicz-Kopec, E., Zwolska, Z., Kirikae, F., Toyota, E., Kobayashi, I., Morita, K., Kudo, K., Kato, S., Kuratsuji, T., Mori, T., Kirikae, T. J. Clin. Microbiol. (2007) [Pubmed]
  3. Mycobacterial catalase-peroxidase is a tissue antigen and target of the adaptive immune response in systemic sarcoidosis. Song, Z., Marzilli, L., Greenlee, B.M., Chen, E.S., Silver, R.F., Askin, F.B., Teirstein, A.S., Zhang, Y., Cotter, R.J., Moller, D.R. J. Exp. Med. (2005) [Pubmed]
  4. Structural characterization of the Ser324Thr variant of the catalase-peroxidase (KatG) from Burkholderia pseudomallei. Deemagarn, T., Carpena, X., Singh, R., Wiseman, B., Fita, I., Loewen, P.C. J. Mol. Biol. (2005) [Pubmed]
  5. Compensatory functions of two alkyl hydroperoxide reductases in the oxidative defense system of Legionella pneumophila. LeBlanc, J.J., Davidson, R.J., Hoffman, P.S. J. Bacteriol. (2006) [Pubmed]
  6. The catalase-peroxidase gene and isoniazid resistance of Mycobacterium tuberculosis. Zhang, Y., Heym, B., Allen, B., Young, D., Cole, S. Nature (1992) [Pubmed]
  7. Ethionamide activation and sensitivity in multidrug-resistant Mycobacterium tuberculosis. DeBarber, A.E., Mdluli, K., Bosman, M., Bekker, L.G., Barry, C.E. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  8. Analysis of heme structural heterogeneity in Mycobacterium tuberculosis catalase-peroxidase (KatG). Chouchane, S., Girotto, S., Kapetanaki, S., Schelvis, J.P., Yu, S., Magliozzo, R.S. J. Biol. Chem. (2003) [Pubmed]
  9. Reduced affinity for Isoniazid in the S315T mutant of Mycobacterium tuberculosis KatG is a key factor in antibiotic resistance. Yu, S., Girotto, S., Lee, C., Magliozzo, R.S. J. Biol. Chem. (2003) [Pubmed]
  10. Purification and characterization of recombinant catalase-peroxidase, which confers isoniazid sensitivity in Mycobacterium tuberculosis. Nagy, J.M., Cass, A.E., Brown, K.A. J. Biol. Chem. (1997) [Pubmed]
  11. Performance of the Genotype MTBDR Line Probe Assay for Detection of Resistance to Rifampin and Isoniazid in Strains of Mycobacterium tuberculosis with Low- and High-Level Resistance. Brossier, F., Veziris, N., Truffot-Pernot, C., Jarlier, V., Sougakoff, W. J. Clin. Microbiol. (2006) [Pubmed]
  12. Public health impact of isoniazid-resistant Mycobacterium tuberculosis strains with a mutation at amino-acid position 315 of katG: a decade of experience in The Netherlands. van Doorn, H.R., de Haas, P.E., Kremer, K., Vandenbroucke-Grauls, C.M., Borgdorff, M.W., van Soolingen, D. Clin. Microbiol. Infect. (2006) [Pubmed]
  13. Hydrogen peroxide-mediated isoniazid activation catalyzed by Mycobacterium tuberculosis catalase-peroxidase (KatG) and its S315T mutant. Zhao, X., Yu, H., Yu, S., Wang, F., Sacchettini, J.C., Magliozzo, R.S. Biochemistry (2006) [Pubmed]
  14. Characterization of the katG and inhA genes of isoniazid-resistant clinical isolates of Mycobacterium tuberculosis. Rouse, D.A., Li, Z., Bai, G.H., Morris, S.L. Antimicrob. Agents Chemother. (1995) [Pubmed]
  15. Resonance Raman spectroscopy of Compound II and its decay in Mycobacterium tuberculosis catalase-peroxidase KatG and its isoniazid resistant mutant S315T. Kapetanaki, S.M., Chouchane, S., Yu, S., Magliozzo, R.S., Schelvis, J.P. J. Inorg. Biochem. (2005) [Pubmed]
  16. Evaluation of the Genotype MTBDR assay for rapid detection of rifampin and isoniazid resistance in Mycobacterium tuberculosis isolates. Cavusoglu, C., Turhan, A., Akinci, P., Soyler, I. J. Clin. Microbiol. (2006) [Pubmed]
  17. Isoniazid's Bactericidal Activity Ceases because of the Emergence of Resistance, Not Depletion of Mycobacterium tuberculosis in the Log Phase of Growth. Gumbo, T., Louie, A., Liu, W., Ambrose, P.G., Bhavnani, S.M., Brown, D., Drusano, G.L. J. Infect. Dis. (2007) [Pubmed]
  18. Use of a mycobacteriophage-based assay for rapid assessment of susceptibilities of Mycobacterium tuberculosis isolates to isoniazid and influence of resistance level on assay performance. Galí, N., Domínguez, J., Blanco, S., Prat, C., Alcaide, F., Coll, P., Ausina, V. J. Clin. Microbiol. (2006) [Pubmed]
  19. Systematic molecular characterization of multidrug-resistant Mycobacterium tuberculosis complex isolates from Spain. Samper, S., Iglesias, M.J., Rabanaque, M.J., Gómez, L.I., Lafoz, M.C., Jiménez, M.S., Ortega, A., Lezcano, M.A., Van Soolingen, D., Martín, C. J. Clin. Microbiol. (2005) [Pubmed]
  20. Role of KatG catalase-peroxidase in mycobacterial pathogenesis: countering the phagocyte oxidative burst. Ng, V.H., Cox, J.S., Sousa, A.O., MacMicking, J.D., McKinney, J.D. Mol. Microbiol. (2004) [Pubmed]
  21. Expression of katG in Mycobacterium tuberculosis is associated with its growth and persistence in mice and guinea pigs. Li, Z., Kelley, C., Collins, F., Rouse, D., Morris, S. J. Infect. Dis. (1998) [Pubmed]
  22. Mutations prevalent among rifampin- and isoniazid-resistant Mycobacterium tuberculosis isolates from a hospital in Vietnam. Caws, M., Duy, P.M., Tho, D.Q., Lan, N.T., Hoa, D.V., Farrar, J. J. Clin. Microbiol. (2006) [Pubmed]
  23. Mycobacterium tuberculosis dihydrofolate reductase is a target for isoniazid. Argyrou, A., Vetting, M.W., Aladegbami, B., Blanchard, J.S. Nat. Struct. Mol. Biol. (2006) [Pubmed]
  24. Population genetics study of isoniazid resistance mutations and evolution of multidrug-resistant Mycobacterium tuberculosis. Hazbón, M.H., Brimacombe, M., Bobadilla del Valle, M., Cavatore, M., Guerrero, M.I., Varma-Basil, M., Billman-Jacobe, H., Lavender, C., Fyfe, J., García-García, L., León, C.I., Bose, M., Chaves, F., Murray, M., Eisenach, K.D., Sifuentes-Osornio, J., Cave, M.D., Ponce de León, A., Alland, D. Antimicrob. Agents Chemother. (2006) [Pubmed]
  25. Molecular characterization of isoniazid-resistant clinical isolates of Mycobacterium tuberculosis from the USA. Guo, H., Seet, Q., Denkin, S., Parsons, L., Zhang, Y. J. Med. Microbiol. (2006) [Pubmed]
  26. Mycobacterium tuberculosis catalase and peroxidase activities and resistance to oxidative killing in human monocytes in vitro. Manca, C., Paul, S., Barry, C.E., Freedman, V.H., Kaplan, G. Infect. Immun. (1999) [Pubmed]
  27. Molecular analysis of Mycobacterium tuberculosis DNA from a family of 18th century Hungarians. Fletcher, H.A., Donoghue, H.D., Taylor, G.M., van der Zanden, A.G., Spigelman, M. Microbiology (Reading, Engl.) (2003) [Pubmed]
  28. Analysis of the oxyR-ahpC region in isoniazid-resistant and -susceptible Mycobacterium tuberculosis complex organisms recovered from diseased humans and animals in diverse localities. Sreevatsan, S., Pan, X., Zhang, Y., Deretic, V., Musser, J.M. Antimicrob. Agents Chemother. (1997) [Pubmed]
  29. Rapid genotypic detection of rifampin- and isoniazid-resistant Mycobacterium tuberculosis directly in clinical specimens. Bang, D., Bengård Andersen, A., Thomsen, V.Ø. J. Clin. Microbiol. (2006) [Pubmed]
  30. Microarray and allele specific PCR detection of point mutations in Mycobacterium tuberculosis genes associated with drug resistance. Tang, X., Morris, S.L., Langone, J.J., Bockstahler, L.E. J. Microbiol. Methods (2005) [Pubmed]
  31. Improving bacteriological diagnosis of tuberculosis. Wattal, C. Indian journal of pediatrics. (2002) [Pubmed]
  32. Modulation of the activities of catalase-peroxidase HPI of Escherichia coli by site-directed mutagenesis. Hillar, A., Peters, B., Pauls, R., Loboda, A., Zhang, H., Mauk, A.G., Loewen, P.C. Biochemistry (2000) [Pubmed]
  33. Conformational differences in Mycobacterium tuberculosis catalase-peroxidase KatG and its S315T mutant revealed by resonance Raman spectroscopy. Kapetanaki, S., Chouchane, S., Girotto, S., Yu, S., Magliozzo, R.S., Schelvis, J.P. Biochemistry (2003) [Pubmed]
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