ArticleBiochemistry2011
Identification of a chemical that inhibits the mycobacterial UvrABC complex in nucleotide excision repair.
Article in Biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 38 citations in OpenAlex.
- Usnic Acid Derivatives as Inhibitors ofInternational journal of molecular sciences · 2026Article
- Isolation and characterization of two new species, Hymenobacter mellowenesis sp. nov. and Hymenobacter aranciens sp. nov., from soil.Archives of microbiology · 2024Article
- Review
- Developing novel antimicrobials by combining cancer chemotherapeutics with bacterial DNA repair inhibitors.PLoS pathogens · 2023Article
- Structural and functional insights into the activation of the dual incision activity of UvrC, a key player in bacterial NER.Nucleic acids research · 2023Article
- Mechanistic insight into the repair of C8-linked pyrrolobenzodiazepine monomer-mediated DNA damage.RSC medicinal chemistry · 2022Article
- Interrogating the substrate specificity landscape of UvrC reveals novel insights into its non-canonical function.Biophysical journal · 2022Article
- Identification of the target and mode of action for the prokaryotic nucleotide excision repair inhibitor ATBC.Bioscience reports · 2022Article
- In vitro reconstitution of an efficient nucleotide excision repair system using mesophilic enzymes from Deinococcus radiodurans.Communications biology · 2022Article
- Targeting Genome Integrity inMolecules (Basel, Switzerland) · 2020Review
- Mycobacterium tuberculosis Molecular Determinants of Infection, Survival Strategies, and Vulnerable Targets.Pathogens (Basel, Switzerland) · 2018Review
- Division of labor among Mycobacterium smegmatis RNase H enzymes: RNase H1 activity of RnhA or RnhC is essential for growth whereas RnhB and RnhA guard against killing by hydrogen peroxide in stationary phase.Nucleic acids research · 2017Article
- Stressed mycobacteria use the chaperone ClpB to sequester irreversibly oxidized proteins asymmetrically within and between cells.Cell host & microbe · 2015Article
- A comparative study of the bactericidal activity and daily disinfection housekeeping surfaces by a new portable pulsed UV radiation device.Current microbiology · 2012Article
- Important role for Mycobacterium tuberculosis UvrD1 in pathogenesis and persistence apart from its function in nucleotide excision repair.Journal of bacteriology · 2012Article
- Enzymatic activities and DNA substrate specificity of Mycobacterium tuberculosis DNA helicase XPB.PloS one · 2012Article
- The biological and structural characterization of Mycobacterium tuberculosis UvrA provides novel insights into its mechanism of action.Nucleic acids research · 2011Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Bacterial DNA can be damaged by reactive nitrogen and oxygen intermediates (RNI and ROI) generated by host immunity, as well as by antibiotics that trigger bacterial production of ROI. Thus a pathogen's ability to repair its DNA may be important for persistent infection. A prominent role for nucleotide excision repair (NER) in disease caused by Mycobacterium tuberculosis (Mtb) was suggested by attenuation of uvrB-deficient Mtb in mice. However, it was unknown if Mtb's Uvr proteins could execute NER. Here we report that recombinant UvrA, UvrB, and UvrC from Mtb collectively bound and cleaved plasmid DNA exposed to ultraviolet (UV) irradiation or peroxynitrite. We used the DNA incision assay to test the mechanism of action of compounds identified in a high-throughput screen for their ability to delay recovery of M. smegmatis from UV irradiation. 2-(5-Amino-1,3,4-thiadiazol-2-ylbenzo[f]chromen-3-one) (ATBC) but not several closely related compounds inhibited cleavage of damaged DNA by UvrA, UvrB, and UvrC without intercalating in DNA and impaired recovery of M. smegmatis from UV irradiation. ATBC did not affect bacterial growth in the absence of UV exposure, nor did it exacerbate the growth defect of UV-irradiated mycobacteria that lacked uvrB. Thus, ATBC appears to be a cell-penetrant, selective inhibitor of mycobacterial NER. Chemical inhibitors of NER may facilitate studies of the role of NER in prokaryotic pathobiology.
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Registered trials
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