ArticleProceedings of the National Academy of Sciences of the United States of America2015
SufB intein of Mycobacterium tuberculosis as a sensor for oxidative and nitrosative stresses.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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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
42 citing papers in PubMed, 65 citations in OpenAlex.
- A protein chaperone can stabilize the intein-containing precursor to indirectly promote protein splicing.Protein science : a publication of the Protein Society · 2026Article
- Designing a Whole-Cell Biosensor for Detection of Toxic Metals Using Intein Splicing Inhibition ofACS omega · 2026Article
- Biofilm Formation in Mycobacterial Genus; Mechanism of Biofilm Formation and Anti-mycobacterial Biofilm Agents.Current pharmaceutical biotechnology · 2025Review
- Controllable intein splicing and N-terminal cleavage at mesophilic temperatures.Frontiers in bioengineering and biotechnology · 2025Article
- Intein splicing efficiency and RadA levels can control the mode of archaeal DNA replication.Science advances · 2024Article
- Conditional protein splicing of the Mycobacterium tuberculosis RecA intein in its native host.Scientific reports · 2024Article
- Conditional protein splicing of thebioRxiv : the preprint server for biology · 2024Article
- Article
- Intein-Mediated Protein Engineering for Cell-Based Biosensors.Biosensors · 2022Review
- SufB intein splicing in Mycobacterium tuberculosis is influenced by two remote conserved N-extein histidines.Bioscience reports · 2022Article
- Conditional Alternative Protein Splicing Promoted by Inteins fromBiochemistry · 2022Article
- Inteins as Drug Targets and Therapeutic Tools.Frontiers in molecular biosciences · 2022Review
- Reactive Chlorine Species Reversibly Inhibit DnaB Protein Splicing in Mycobacteria.Microbiology spectrum · 2021Article
- Monitoring Protein Splicing Using In-gel Fluorescence Immediately Following SDS-PAGE.Bio-protocol · 2021Article
- Transcriptomics Analysis Uncovers Transient Ceftazidime Tolerance inACS infectious diseases · 2021Article
- Construction and Quantitation of a Selectable Protein Splicing Sensor Using Gibson Assembly and Spot Titers.Current protocols · 2021Article
- Intein Inhibitors as Novel Antimicrobials: Protein Splicing in Human Pathogens, Screening Methods, and Off-Target Considerations.Frontiers in molecular biosciences · 2021Review
- Gold Nanoparticles Augment N-Terminal Cleavage and Splicing Reactions inFrontiers in bioengineering and biotechnology · 2021Article
- Inteins in Science: Evolution to Application.Microorganisms · 2020Review
- Protein Splicing Activity of theBiochemistry · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Inteins are mobile genetic elements that self-splice at the protein level. Mycobacteria have inteins inserted into several important genes, including those corresponding to the iron-sulfur cluster assembly protein SufB. Curiously, the SufB inteins are found primarily in mycobacterial species that are potential human pathogens. Here we discovered an exceptional sensitivity of Mycobacterium tuberculosis SufB intein splicing to oxidative and nitrosative stresses when expressed in Escherichia coli. This effect results from predisposition of the intein's catalytic cysteine residues to oxidative and nitrosative modifications. Experiments with a fluorescent reporter system revealed that reactive oxygen species and reactive nitrogen species inhibit SufB extein ligation by forcing either precursor accumulation or N-terminal cleavage. We propose that splicing inhibition is an immediate, posttranslational regulatory response that can be either reversible, by inducing precursor accumulation, or irreversible, by inducing N-terminal cleavage, which may potentially channel mycobacteria into dormancy under extreme oxidative and nitrosative stresses.
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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.