inhA Antibody

1. Out of the 141 isolates studied, 3 (2.1%) were found carrying mutations in the katG gene that confer resistance to Isoniazid (INH). No mutations were detected in the inhA promoter region gene that confer weak INH resistance or in the rpoB gene that confer Rifampicin resistance. PMID: 29868151
2. Molecular dynamics (MD) simulation show that EN and N1 remained in the binding pocket similar to the docked pose of EN-InhA and E1-InhA complexes and also suggested that InhA binds to its inhibitor in inhibitor-induced folding manner. Our study concludes that multiple receptor conformers based molecular docking can be an alternative to study the effect of receptor flexibility in ligand binding PMID: 28957755
3. Virtually Designed Triclosan-Based Inhibitors of Enoyl-Acyl Carrier Protein Reductase of Mycobacterium tuberculosis and of Plasmodium falciparum. PMID: 27490275
4. Structural analysis of InhA provided the crucial points to enhance the NADH binding affinity towards InhA mutants in the presence of direct InhA inhibitors to combat isoniazid drug resistance. PMID: 26658674
5. InhA gene mutation is associated with isoniazid resistance in Mycobacterium tuberculosis. PMID: 25799046
6. The specific zone mutations in inhA gene for rifampicin and isoniazid were investigated with molecular methods in isolated unique PMID: 26506671
7. Rational Modulation of the Induced-Fit Conformational Change for Slow-Onset Inhibition in Mycobacterium tuberculosis InhA. PMID: 26147157
8. The study reports empirical parameters to differentiate the 'open' and 'closed' conformation of substrate-binding loop by comprehensive ana-lysis of InhA crystal structures. PMID: 24895891
9. The results reveal that the presence of a mutation in the inhA regulatory region together with a mutation in the inhA coding region can lead to the development of high-level isoniazid resistance and cross-resistance to ethionamide among the MDR-TB strains circulating in Lisbon. PMID: 23539241
10. No mutation was observed in the inhA promotor region or in the INH sensitive control isolate (H37Rv). PMID: 22358357
11. We chose to search for new inhibitors of the enoyl-acyl carrier protein reductase InhA, the target of the first-line TB drug isoniazid. Two compounds (CD39 and CD117) were bactericidal against drug-susceptible and drug-resistant M. tuberculosis. PMID: 21628538
12. inhA promoter mutations are strongly associated with extensively drug-resistant-tuberculosis in South Africa PMID: 21333101
13. Phosphorylation of InhA inhibits mycolic acid biosynthesis and growth of Mycobacterium tuberculosis. PMID: 21143326
14. InhA phosphorylation is an important event in regulating cell growth. PMID: 20864541
15. inhA(S94A) allele confers clinically relevant levels of resistance to isoniazid killing & inhibition of mycolic acid synthesis. decreased binding of INH-NAD inhibitor to InhA establishes InhA as primary target of isoniazid action in M. tuberculosis. PMID: 16906155
16. catalysis of substrate reduction by InhA results, in part, from correct orientation of the cofactor in the ground state PMID: 17472376
17. T (-8)C of inhA mutations was found in multidrug resistant Mycobacterium tuberculosis isolates. PMID: 17539290
18. The structure of two InhA mutants (I21V and S94A), identified in INH-resistant clinical isolates, were solved. PMID: 17588773
19. inhibited by Anthecotulide from Anthemis auriculata PMID: 18424102

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KEGG: mtu:Rv1484

STRING: 83332.Rv1484