<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sarrazin M</submitter><funding>Agence Nationale de la Recherche</funding><funding>Association Vaincre la Mucoviscidose</funding><pagination>103</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11613490</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>31(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Mycobacterium abscessus is an emerging pathogen causing severe pulmonary infections, particularly in individuals with underlying conditions, such as cystic fibrosis or chronic obstructive pulmonary disease. Macrolides, such as clarithromycin (CLR) or azithromycin (AZM), represent the cornerstone of antibiotherapy against the M. abscessus species. However, prolonged exposure to these macrolides can induce of Erm(41)-mediated resistance, limiting their spectrum of activity and leading to therapeutic failure. Therefore, inhibiting Erm(41) could thwart this resistance mechanism to maintain macrolide susceptibility, thus increasing the rate of treatment success. In our previous study, the Erm(41) methyltransferase was identified as a possible target enzyme of Cyclipostins and</pubmed_abstract><journal>Journal of biomedical science</journal><pubmed_title>Cyclophostin and Cyclipostins analogues counteract macrolide-induced resistance mediated by erm(41) in Mycobacterium abscessus.</pubmed_title><pmcid>PMC11613490</pmcid><funding_grant_id>RF20220503053</funding_grant_id><funding_grant_id>RF20190502466</funding_grant_id><funding_grant_id>19-CE44- 0011</funding_grant_id><pubmed_authors>Sarrazin M</pubmed_authors><pubmed_authors>Santucci P</pubmed_authors><pubmed_authors>Spilling CD</pubmed_authors><pubmed_authors>Herrmann JL</pubmed_authors><pubmed_authors>Poncin I</pubmed_authors><pubmed_authors>Camoin L</pubmed_authors><pubmed_authors>Fourquet P</pubmed_authors><pubmed_authors>Kremer L</pubmed_authors><pubmed_authors>Denis Y</pubmed_authors><pubmed_authors>Le Moigne V</pubmed_authors><pubmed_authors>Cavalier JF</pubmed_authors><pubmed_authors>Canaan S</pubmed_authors><pubmed_authors>Audebert S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cyclophostin and Cyclipostins analogues counteract macrolide-induced resistance mediated by erm(41) in Mycobacterium abscessus.</name><description>&lt;h4>Background&lt;/h4>Mycobacterium abscessus is an emerging pathogen causing severe pulmonary infections, particularly in individuals with underlying conditions, such as cystic fibrosis or chronic obstructive pulmonary disease. Macrolides, such as clarithromycin (CLR) or azithromycin (AZM), represent the cornerstone of antibiotherapy against the M. abscessus species. However, prolonged exposure to these macrolides can induce of Erm(41)-mediated resistance, limiting their spectrum of activity and leading to therapeutic failure. Therefore, inhibiting Erm(41) could thwart this resistance mechanism to maintain macrolide susceptibility, thus increasing the rate of treatment success. In our previous study, the Erm(41) methyltransferase was identified as a possible target enzyme of Cyclipostins and</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2026-06-03T05:21:03.537Z</modification><creation>2025-04-04T02:36:10.934Z</creation></dates><accession>S-EPMC11613490</accession><cross_references><pubmed>39623375</pubmed><doi>10.1186/s12929-024-01091-w</doi></cross_references></HashMap>