<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8</volume><submitter>Giddey AD</submitter><funding>National Research Foundation</funding><pubmed_abstract>Despite the availability of effective drug treatment, &lt;i>Mycobacterium tuberculosis&lt;/i> (Mtb), the causative agent of TB disease, kills ~1. 5 million people annually, and the rising prevalence of drug resistance increasingly threatens to worsen this plight. We previously showed that sublethal exposure to the frontline anti-TB drug, rifampicin, resulted in substantial adaptive remodeling of the proteome of the model organism, &lt;i>Mycobacterium smegmatis&lt;/i>, in the drug-sensitive mc&lt;sup>2&lt;/sup>155 strain [wild type (WT)]. In this study, we investigate whether these responses are conserved in an engineered, isogenic mutant harboring the clinically relevant S531L rifampicin resistance-conferring mutation (SL) and distinguish the responses that are specific to RNA polymerase β subunit- (RpoB-) </pubmed_abstract><journal>Frontiers in medicine</journal><pagination>723667</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8525676</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Cell Wall Proteomics Reveal Phenotypic Adaption of Drug-Resistant &lt;i>Mycobacterium smegmatis&lt;/i> to Subinhibitory Rifampicin Exposure.</pubmed_title><pmcid>PMC8525676</pmcid><pubmed_authors>Soares NC</pubmed_authors><pubmed_authors>Ganief TA</pubmed_authors><pubmed_authors>Blackburn JM</pubmed_authors><pubmed_authors>Ganief N</pubmed_authors><pubmed_authors>Koch A</pubmed_authors><pubmed_authors>Giddey AD</pubmed_authors><pubmed_authors>Warner DF</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cell Wall Proteomics Reveal Phenotypic Adaption of Drug-Resistant &lt;i>Mycobacterium smegmatis&lt;/i> to Subinhibitory Rifampicin Exposure.</name><description>Despite the availability of effective drug treatment, &lt;i>Mycobacterium tuberculosis&lt;/i> (Mtb), the causative agent of TB disease, kills ~1. 5 million people annually, and the rising prevalence of drug resistance increasingly threatens to worsen this plight. We previously showed that sublethal exposure to the frontline anti-TB drug, rifampicin, resulted in substantial adaptive remodeling of the proteome of the model organism, &lt;i>Mycobacterium smegmatis&lt;/i>, in the drug-sensitive mc&lt;sup>2&lt;/sup>155 strain [wild type (WT)]. In this study, we investigate whether these responses are conserved in an engineered, isogenic mutant harboring the clinically relevant S531L rifampicin resistance-conferring mutation (SL) and distinguish the responses that are specific to RNA polymerase β subunit- (RpoB-) </description><dates><release>2021-01-01T00:00:00Z</release><publication>2021</publication><modification>2026-05-08T02:16:04.866Z</modification><creation>2024-11-15T17:46:52.582Z</creation></dates><accession>S-EPMC8525676</accession><cross_references><pubmed>34676224</pubmed><doi>10.3389/fmed.2021.723667</doi></cross_references></HashMap>