katG Antibody

1. Mycobacterium tuberculosis resistance to isoniazid emerges via key mutations in KatG, resulting in constriction of one or more access channels from the KatG surface to the buried catalytic center. PMID: 29523317
2. The katG mutant gene conferring resistance to INH was the only genomic mutation observed among the isolates studied and the frequency of occurrence was low. All katG mutant genes had a S315T1 single point mutation, a genomic alteration that mediates high INH resistance. PMID: 29868151
3. The substitutions of T354I and G421S in mutant katG R2 created significant instability in the adduct triad complex (Trp107-Tyr229-Met255), a part of the active site of the catalase-peroxidase enzyme in the model structure analysis. PMID: 30140323
4. This work evaluated ten point mutations described in the enzyme KatG that are related to resistance to INH (isoniazid). It was showed that the resistance mechanism is related to stereochemical modifications at the N-terminal domain of the protein, which restrict INH access to its catalytic site, not involving mechanisms of electrostatic nature. PMID: 28303436
5. possible functional variation in isoniazid and rifampicin resistance with respect to the identified mutations in KatG and rpoB genes PMID: 28245964
6. Report the active binding site of isoniazid and provide new insight about the conformational changes in the binding site of S315T-MtKatG. PMID: 28610784
7. Mutations in rpoB and in katG are mainly responsible for the multidrug resistance of Mycobacterium tuberculosis. PMID: 28900077
8. Detection of katG and inhA mutations can be used to guide isoniazid and ethionamide use for drug-resistant tuberculosis. PMID: 27393546
9. The loss of the salt bridge in the substrate binding site in mutant KatG Asn238Ser creates changes unfavorable for enzyme activities, which confers isonizid resistance to M. tuberculosis. PMID: 29235814
10. Mutations were found at the frequency of 41.9% for katG, 25.6% for inhA, and 69.8% for rpoB genes in multidrug-resistant strains. Multimarker analysis revealed that combination of only two mutations ("katG/S315T+rpoB/S531L") was a better surrogate of multidrug-resistant tuberculosis than single-marker analysis (86% sensitivity vs. 62.8%). PMID: 26874220
11. Mutations in codon 315 of the katG gene were most common in rifampicin- and isoniazid-resistant strains of Mycobacterium tuberculosis sputum specimens from patients with pulmonary tuberculosis. PMID: 27534023
12. The greatest rate of mutations causing ethionamide resistance were observed in katG, ethA, in mshA. PMID: 26369965
13. There is a requirement for functional katG-encoded catalase-peroxide in the slow growers but not the fast-growing bacteria, which may explain why katG codon Ser315 mutations are favoured in the slow growing cultures. PMID: 26382066
14. Totally mutations in the katG gene were identified in 13 paired isolates Those results showed that the different test systems and the mixed infection with particular genotypes of M. tuberculosis strains contributed to the drug susceptibility discrepancies PMID: 26064938
15. The specific zone mutations in katG gene for rifampicin and isoniazid were investigated with molecular methods in isolated unique strains from patients diagnosed with pulmonary tuberculosis. PMID: 26506671
16. Mutations at codon 315 within the katG gene, depending on their type might be useful for the prediction of isoniazid resistance in Mycobacterium tuberculosis. PMID: 23744165
17. The katG Ser315Thr mutation is one of the main causes of resistance to isoniazid in MDRTB L-form isolates PMID: 24626681
18. The S315T mutation in the katG gene is the predominant mechanism of isoniazid resistance in our circulating strains. PMID: 23412028
19. Most isoniazid-resistant TB cases with non-katG mutations have disease associated with faster response to treatment, and most cases with katG mutants have localized lung involvement. PMID: 23453008
20. Investigated rpoB and katG mutations in rifampicin and isoniazid resistant strains of M. tuberculosis circulating in Northern India and the utility of multiplex-allele-specific PCR assay for detection of drug-resistant MTB isolates in low resource set up. PMID: 23325741
21. In the Mycobacterium catalase, KatG, release of molecular oxygen and regeneration of resting enzyme catalyzed in the last step of the proposed reaction mechanism. PMID: 22918833
22. Among the total 107 isoniazid resistant isolates, the mutation located in katG gene was 98.1% (105/107) and in inhA MUT1 gene was (16.8%; 18/107). PMID: 22808802
23. Ser315Thr mutaion of KatG could be a potential genetic marker for predicting Multidrug resistant tuberculosis PMID: 22610803
24. The sequencing of the 250 bp region of katG codon 315 revealed point mutations at 5 different codons in 13.7% of the 80 MTB isolates PMID: 22358357
25. Multi-mutated isolates found to have combination of mutations with nucleotide changes in codons 315, 316, 309 also demonstrated to be more frequent in isolates of patients with secondary infections bearing higher level of resistance to isoniazid. PMID: 21554227
26. mechanism of the time-dependent transition from one high spin ferric haem form to another must be more complex than a simple single site oxidation. PMID: 22381358
27. Findings suggest that OxyS is a negative regulator of katG in mycobacteria. PMID: 22272299
28. Hotspot mutations within the katG 315 and inhA-15 genes can be used as genetic markers for detection of isoniazid resistance. PMID: 21388297
29. Downregulation of katG expression is associated with isoniazid resistance. PMID: 21244531
30. 9 novel KatG mutants with a single-amino-acid substitution were found; all mutants had lower INH oxidase activities than wild type and each had various levels of activity; isolates with mutations with relatively low activity had high-level INH resistance PMID: 20211896
31. the catalytic properties of the wild-type enzyme to 23 KatG mutants which have been associated with isoniazid resistance in clinical M. tuberculosis isolates were compared. PMID: 20054829
32. Drug resistance in M tuberculosis is due to mutations in relatively restricted regions of the genome: rpoB for RIF, katG and inhA for INH, embB for ethambutol, pncA for pyrazinamide, and so on. PMID: 19741059
33. the analysis of region 1 results in an increase in the rate at which the genotypic diagnosis of INH resistance-arising from mutations, deletions or insertions in the katG gene-is reached. PMID: 19750330
34. S315T mutation seems to induce small changes in the KatG conformation/dynamics of the ligand access channel. PMID: 15628865
35. the Met-Tyr-Trp cross-link in KatG is formed through an autocatalytic mechanism and has an effect on enzyme catalysis and spectroscopic properties PMID: 15840564
36. insight into contributions of the individual Tyr-Trp and Met-Tyr cross-links to catalase activity is presented & the contribution of the Met-Tyr-Trp cross-link to the structure-function-spectroscopy relationship and catalase-peroxidase mechanism in KatG PMID: 16285713
37. data demonstrate physiologically relevant explanation of the mechanism for the bactericidal effect of isoniazid(INH) resulting from the role of KatG in INH activation consistent with structural & functional properties of wild-type & drug-resistant enzyme PMID: 16566587
38. Results are consistent with formation of a tyr radical assigned to residue Tyr(229) within the first few milliseconds of turnover. This is followed by a mixture of tyr and trp radical species and finally to only a tyrosyl radical on residue Tyr(353). PMID: 17204474
39. rapid kinetic and spectral analysis of the reactions of KatGs from three different sources (Synechocystis PCC 6803, Burkholderia pseudomallei, and Mycobacterium tuberculosis) with peroxoacetic acid and hydrogen peroxide PMID: 17260948
40. The binding of INH and a series of hydrazide analogues to resting KatG was examined using optical and calorimetric techniques to provide thermodynamic parameters, binding stoichiometries, and kinetic constants (on and off rates). PMID: 17309235
41. Trp308Pro of KatG mutation was found in multidrug resistant Mycobacterium tuberculosis. PMID: 17539290
42. All isoniazid-resistant Mycobacterium tuberculosis isolates from patients in Belarus had resistance-associated changes, mostly in codons 315(95%), 316(16.2%) and 309(14.5%). PMID: 17978919
43. both a polypurine sequence & translation initiation contribute to mRNA stability. furA-katG mRNA is transcribed from furA promoter & immediately processed; processing is prevented by double stranded RNA at the cutting site. PMID: 18394163
44. Direct evidence reveals that lung and blood T-cell responses to KatG in two cohorts of sarcoidosis patients are regulated in a manner expected for a candidate pathogenic antigen. PMID: 19050300
45. Role of the oxyferrous heme intermediate and distal side adduct radical in the catalase activity of Mycobacterium tuberculosis KatG revealed by the W107F mutant PMID: 19139098
46. An oxyferrous heme/protein-based radical intermediate is catalytically competent in the catalase reaction of Mycobacterium tuberculosis catalase-peroxidase (KatG). PMID: 19139099
47. Multidrug resistance of MBT to rifampicin and isoniazid was mainly due to the combined mutation Ser531 --> Leu in the rpoB gene and to the mutation Ser315 --> Thr in the katG gene. PMID: 19334480

Show More

Hide All

KEGG: mtu:Rv1908c

STRING: 83332.Rv1908c