ArticleACS infectious diseases2019
Direct Inhibition of MmpL3 by Novel Antitubercular Compounds.
Article in ACS infectious diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
66 citing papers in PubMed, 96 citations in OpenAlex.
- The polar landscape of bacterial pathogens and predators.Current opinion in microbiology · 2026Review
- Phytochemical Analysis and Bioactivities ofPlants (Basel, Switzerland) · 2026Article
- Multidrug-resistant tuberculosis: a comprehensive review of pathogenesis, drug resistance, current treatment and future prospects.Archives of microbiology · 2026Review
- Ιdentification of SQ109 analogs with enhanced antimicrobial activity against methicillin-resistantAntimicrobial agents and chemotherapy · 2026Article
- Reference-based chemical-genetic interaction profiling to elucidate small molecule mechanism of action in Mycobacterium tuberculosis.Nature communications · 2025Article
- Microbiological evidence for the trisubstituted benzimidazoles targeting MmpL3 inAntimicrobial agents and chemotherapy · 2025Article
- MmpL12 transports lipooligosaccharides and impacts virulence inMicrobiology (Reading, England) · 2025Article
- Mycolic Acid-like Lipids Act as Substrates forACS omega · 2025Article
- Common Biological Properties ofACS infectious diseases · 2025Article
- Integration of multi-modal measurements identifies critical mechanisms of tuberculosis drug action.Cell systems · 2025Article
- Investigating the unbinding mechanisms and kinetics of MmpL3 inhibitors: A computational study.Protein science : a publication of the Protein Society · 2025Article
- Tailored phenyl ureas eradicate drug-resistantChemical science · 2025Article
- Structural modeling and characterization of the Mycobacterium tuberculosis MmpL3 C-terminal domain.FEBS letters · 2024Article
- MmpL3, Wag31, and PlrA are involved in coordinating polar growth with peptidoglycan metabolism and nutrient availability.Journal of bacteriology · 2024Article
- The conserved σD envelope stress response monitors multiple aspects of envelope integrity in corynebacteria.PLoS genetics · 2024Article
- Therapeutic developments for tuberculosis and nontuberculous mycobacterial lung disease.Nature reviews. Drug discovery · 2024Review
- MmpL3, Wag31 and PlrA are involved in coordinating polar growth with peptidoglycan metabolism and nutrient availability.bioRxiv : the preprint server for biology · 2024Article
- Molecular insights into the determinants of substrate specificity and efflux inhibition of the RND efflux pumps AcrB and AdeB.Microbiology (Reading, England) · 2024Review
- S288T mutation altering MmpL3 periplasmic domain channel and H-bond network: a novel dual drug resistance mechanism.Journal of molecular modeling · 2024Article
- Discovery, Synthesis, and Optimization of 1,2,4-Triazolyl Pyridines TargetingACS infectious diseases · 2023Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
MmpL3, an essential transporter involved in the export of mycolic acids, is the proposed target of a number of antimycobacterial inhibitors under development. Whether MmpL3 serves as the direct target of these compounds, however, has been called into question after the discovery that some of them dissipated the proton motive force from which MmpL transporters derive their energy. Using a combination of in vitro and whole-cell-based approaches, we here provide evidence that five structurally distinct MmpL3 inhibitor series, three of which impact proton motive force in Mycobacterium tuberculosis, directly interact with MmpL3. Medium- to high-throughput assays based on these approaches were developed to facilitate the future screening and optimization of MmpL3 inhibitors. The promiscuity of MmpL3 as a drug target and the mechanisms through which missense mutations located in a transmembrane region of this transporter may confer cross-resistance to a variety of chemical scaffolds are discussed in light of the exquisite vulnerability of MmpL3, its apparent mechanisms of interaction with inhibitors, and evidence of conformational changes induced both by the inhibitors and one of the most commonly identified resistance mutations in MmpL3.
Indexed as
Identifiers
What OpenQuestion holds
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.