ArticleInfection and immunity2005
Role for nucleotide excision repair in virulence of Mycobacterium tuberculosis.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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.
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
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- Identification of gene targets against dormant phase Mycobacterium tuberculosis infections.BMC infectious diseases · 2007Pooled it
- Deleting the 2B domain of mycobacterial UvrD1 unmasks a latent helicase activity in vitro but effaces UvrD1 activity in nucleotide excision repair in vivo.Nucleic acids research · 2026Article
- Mechanistic understanding of UvrA damage detection and lesion hand-off to UvrB in Nucleotide Excision Repair.Nature communications · 2025Article
- In vivo nucleotide excision repair by mycobacterial UvrD1 requires ATP hydrolysis but does not depend on cysteine disulfide-mediated dimerization and DNA unwinding.Nucleic acids research · 2025Article
- Prominent transcriptomic changes in Mycobacterium intracellulare under acidic and oxidative stress.BMC genomics · 2024Article
- Transcriptional Profiling of Homologous Recombination Pathway Genes inMicroorganisms · 2023Article
- Interrogating the substrate specificity landscape of UvrC reveals novel insights into its non-canonical function.Biophysical journal · 2022Article
- Distinctive roles of translesion polymerases DinB1 and DnaE2 in diversification of the mycobacterial genome through substitution and frameshift mutagenesis.Nature communications · 2022Article
- Identification of the target and mode of action for the prokaryotic nucleotide excision repair inhibitor ATBC.Bioscience reports · 2022Article
- Article
- Division of labor between SOS and PafBC in mycobacterial DNA repair and mutagenesis.Nucleic acids research · 2021Article
- Integrated sensing of host stresses by inhibition of a cytoplasmic two-component system controlseLife · 2021Article
- Use of Ultraviolet Blood Irradiation Against Viral Infections.Clinical reviews in allergy & immunology · 2021Review
- Global Assessment of Mycobacterium avium subsp.mSystems · 2019Article
- Identification of Missing Carbon Fixation Enzymes as Potential Drug Targets in Mycobacterium Tuberculosis.Journal of integrative bioinformatics · 2018Article
- Kunkel Lecture: Fundamental immunodeficiency and its correction.The Journal of experimental medicine · 2017Review
- DNA Replication in Mycobacterium tuberculosis.Microbiology spectrum · 2017Review
- Physiology, Biochemistry, and Applications of F420- and Fo-Dependent Redox Reactions.Microbiology and molecular biology reviews : MMBR · 2016Review
- Article
- E1 of α-ketoglutarate dehydrogenase defends Mycobacterium tuberculosis against glutamate anaplerosis and nitroxidative stress.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in Mycobacterium tuberculosis uvrB result in severe sensitivity to acidified nitrite, a source of nitric oxide (6). In this study, we show that a uvrB mutant is exquisitely sensitive to UV light but not to several sources of reactive oxygen species in vitro. Furthermore, a uvrB mutant was attenuated in mice as judged by an extension of life span. Attenuation in mice was partially reversed by genetic inactivation of nitric oxide synthase 2 (iNOS) and almost completely reversed in mice lacking both iNOS and phagocyte oxidase. Thus, a gene predicted to encode a key element of DNA repair is required for resistance of M. tuberculosis to both reactive nitrogen and reactive oxygen species in mice.
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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.