M. tuberculosis Transcription Machinery: A Review on the Mycobacterial RNA Polymerase and Drug Discovery Efforts.

Keywords: M. tuberculosis; DNA-dependent RNA polymerase; transcription inhibition EN M. tuberculosis DNA-dependent RNA polymerase transcription inhibition 1774 21 11/17/22 20221101 NES 221101 1. The activity of RIF is lowered due to the increase in multi-drug resistance/RIF resistance TB (MDR/RR-TB) strains from mutations in the RIF binding site of RpoB, which results in structural incompatibility and treatment failure [[21]]. For example, RIF sensitivity towards MTB RNAP is 1000-fold higher compared to I E. coli i RNAP, although RIF was found to bind tightly to the same binding site in I E. coli i RNAP [[19]]. In M. stegmatis, RbpA influences RIF affinity towards the RNAP binding site and increases the resistance level due to the proximity of I M. stegmatis i and RbpA binding site (residue R381 on the subunit) to the RIF binding site on the subunit [[77]]. RIF, the first line drug for TB, belongs to this category and binds to the RIF binding site adjacent to the RNAP active site, sterically blocking the growth of newly synthesized RNA transcript after 2-3 nucleotides. [Extracted from the article]

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