ArticlePLoS pathogens2016
Mycobacterium tuberculosis Thioredoxin Reductase Is Essential for Thiol Redox Homeostasis but Plays a Minor Role in Antioxidant Defense.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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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Who cites it
49 citing papers in PubMed, 78 citations in OpenAlex.
- Targeting thioredoxin reductase for anti-tuberculosis drug discovery: the inhibitor OSSL_632214.Applied microbiology and biotechnology · 2026Article
- Multidrug-resistant tuberculosis: a comprehensive review of pathogenesis, drug resistance, current treatment and future prospects.Archives of microbiology · 2026Review
- Lactobacillus-derived extracellular vesicles provide multi-target acne treatment by enriched proteins and skin microbiota protection.Journal of nanobiotechnology · 2026Article
- Future Research Directions on Mycobacterium tuberculosis Proteins.Advances in experimental medicine and biology · 2026Review
- Recent Characterization of Key Proteins to Combat Tuberculosis.Advances in experimental medicine and biology · 2026Review
- Role of thioredoxin reductase (TrxB) in oxidative stress response ofJournal of bacteriology · 2025Article
- Integration of multi-modal measurements identifies critical mechanisms of tuberculosis drug action.Cell systems · 2025Article
- Design and Development of Lysyl tRNA Synthetase Inhibitors, for the Treatment of Tuberculosis.Journal of medicinal chemistry · 2025Article
- Redox Imbalance in Inflammation: The Interplay of Oxidative and Reductive Stress.Antioxidants (Basel, Switzerland) · 2025Review
- Whole genome CRISPRi screening identifies druggable vulnerabilities in an isoniazid resistant strain of Mycobacterium tuberculosis.Nature communications · 2024Article
- Intracellular peroxynitrite perturbs redox balance, bioenergetics, and Fe-S cluster homeostasis in Mycobacterium tuberculosis.Redox biology · 2024Review
- Exploring Immune Redox Modulation in Bacterial Infections: Insights into Thioredoxin-Mediated Interactions and Implications for Understanding Host-Pathogen Dynamics.Antioxidants (Basel, Switzerland) · 2024Review
- A Chemoproteomic Approach to Elucidate the Mechanism of Action of 6-Azasteroids with Unique Activity in Mycobacteria.ACS infectious diseases · 2023Article
- The role of thioredoxin proteins inBiochemistry and biophysics reports · 2023Article
- Novel starting points for fragment-based drug design against mycobacterial thioredoxin reductase identified using crystallographic fragment screening.Acta crystallographica. Section D, Structural biology · 2023Article
- Working together to fighting the bad guys.microLife · 2023Article
- Types and functions of heterogeneity in mycobacteria.Nature reviews. Microbiology · 2022Review
- Deciphering the Proteomic Landscape ofACS omega · 2022Article
- Molecular Connectivity between Extracytoplasmic Sigma Factors and PhoP Accounts for Coupled Mycobacterial Stress Response.Journal of bacteriology · 2022Article
- Clinically encountered growth phenotypes of tuberculosis-causing bacilli and theirFrontiers in cellular and infection microbiology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Mycobacterium tuberculosis (Mtb) must cope with exogenous oxidative stress imposed by the host. Unlike other antioxidant enzymes, Mtb's thioredoxin reductase TrxB2 has been predicted to be essential not only to fight host defenses but also for in vitro growth. However, the specific physiological role of TrxB2 and its importance for Mtb pathogenesis remain undefined. Here we show that genetic inactivation of thioredoxin reductase perturbed several growth-essential processes, including sulfur and DNA metabolism and rapidly killed and lysed Mtb. Death was due to cidal thiol-specific oxidizing stress and prevented by a disulfide reductant. In contrast, thioredoxin reductase deficiency did not significantly increase susceptibility to oxidative and nitrosative stress. In vivo targeting TrxB2 eradicated Mtb during both acute and chronic phases of mouse infection. Deliberately leaky knockdown mutants identified the specificity of TrxB2 inhibitors and showed that partial inactivation of TrxB2 increased Mtb's susceptibility to rifampicin. These studies reveal TrxB2 as essential thiol-reducing enzyme in Mtb in vitro and during infection, establish the value of targeting TrxB2, and provide tools to accelerate the development of TrxB2 inhibitors.
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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.