ArticlePloS one2013
Mab_3168c, a putative acetyltransferase, enhances adherence, intracellular survival and antimicrobial resistance of Mycobacterium abscessus.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Functional characterization of GplA (MSMEG-0394) reveals a novel determinant of glycopeptidolipids homeostasis inFrontiers in microbiology · 2026Article
- Sources, transmission and hospital-associated outbreaks of nontuberculous mycobacteria: a review.Future microbiology · 2024Review
- 10-DEBC Hydrochloride as a Promising New Agent against Infection ofInternational journal of molecular sciences · 2022Article
- Virulence Mechanisms ofFrontiers in microbiology · 2022Review
- Article
- Non-Tuberculous Mycobacteria: Molecular and Physiological Bases of Virulence and Adaptation to Ecological Niches.Microorganisms · 2020Review
- Article
- The extracellular matrix of mycobacterial biofilms: could we shorten the treatment of mycobacterial infections?Microbial cell (Graz, Austria) · 2019Review
- Lack of antimicrobial bactericidal activity in Mycobacterium abscessus.Antimicrobial agents and chemotherapy · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium abscessus is a non-tuberculous mycobacterium. It can cause diseases in both immunosuppressed and immunocompetent patients and is highly resistant to multiple antimicrobial agents. M. abscessus displays two different colony morphology types: smooth and rough morphotypes. Cells with a rough morphotype are more virulent. The purpose of this study was to identify genes responsible for M. abscessus morphotype switching. With transposon mutagenesis, a mutant with a Tn5 inserted into the promoter region of the mab_3168c gene was found to switch its colonies from a rough to a smooth morphotype. This mutant had a higher sliding motility but a lower ability to form biofilms, aggregate in culture, and survive inside macrophages. Results of bioinformatic analyses suggest that the putative Mab_3168c protein is a member of the GCN5-related N-acetyltransferase superfamily. This prediction was supported by the demonstration that the mab_3168c gene conferred M. abscessus and M. smegmatis cells resistance to amikacin. The multiple roles of mab_3168c suggest that it could be a potential target for development of therapeutic regimens to treat diseases caused by M. abscessus.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.