{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pal P"],"funding":["Council of Scientific and Industrial Research","Department of Biotechnology, Ministry of Science and Technology"],"pagination":["708"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10336103"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["6(1)"],"pubmed_abstract":["Survival response of the human tuberculosis pathogen, Mycobacterium tuberculosis (Mtb) to a diverse environmental cues is governed through its versatile transcription regulatory mechanisms with the help of a large pool of transcription regulators (TRs). Rv1830 is one such conserved TR, which remains uncharacterized in Mtb. It was named as McdR based on an effect on cell division upon its overexpression in Mycobacterium smegmatis. Recently, it has been implicated in antibiotic resilience in Mtb and reannotated as ResR. While Rv1830 affects cell division by modulating the expression of M. smegmatis whiB2, the underlying cause of its essentiality and regulation of drug resilience in Mtb is yet to be deciphered. Here we show that ResR/McdR, encoded by ERDMAN_2020 in virulent Mtb Erdman, is piv"],"journal":["Communications biology"],"pubmed_title":["ResR/McdR-regulated protein translation machinery contributes to drug resilience in Mycobacterium tuberculosis."],"pmcid":["PMC10336103"],"funding_grant_id":["BT/PR25690/GET/119/142/2017","15/12/2019 (ii) EU-V"],"pubmed_authors":["Agarwal N","Sharma S","Kumar Y","Khan MY","Mangla N","Kaushal PS","Pal P"],"additional_accession":[]},"is_claimable":false,"name":"ResR/McdR-regulated protein translation machinery contributes to drug resilience in Mycobacterium tuberculosis.","description":"Survival response of the human tuberculosis pathogen, Mycobacterium tuberculosis (Mtb) to a diverse environmental cues is governed through its versatile transcription regulatory mechanisms with the help of a large pool of transcription regulators (TRs). Rv1830 is one such conserved TR, which remains uncharacterized in Mtb. It was named as McdR based on an effect on cell division upon its overexpression in Mycobacterium smegmatis. Recently, it has been implicated in antibiotic resilience in Mtb and reannotated as ResR. While Rv1830 affects cell division by modulating the expression of M. smegmatis whiB2, the underlying cause of its essentiality and regulation of drug resilience in Mtb is yet to be deciphered. Here we show that ResR/McdR, encoded by ERDMAN_2020 in virulent Mtb Erdman, is piv","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jul","modification":"2026-04-29T02:34:01.456Z","creation":"2025-02-19T04:02:17.357Z"},"accession":"S-EPMC10336103","cross_references":{"pubmed":["37433855"],"doi":["10.1038/s42003-023-05059-8"]}}