ArticleTuberculosis (Edinburgh, Scotland)2009
Mycobacterium tuberculosis ftsH expression in response to stress and viability.
Article in Tuberculosis (Edinburgh, Scotland), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 23 citations in OpenAlex.
- Close Related Drug-Resistance Beijing Isolates ofInternational journal of molecular sciences · 2022Article
- Genomic and Transcriptomic Analysis of BovineFrontiers in veterinary science · 2021Article
- Local adaptive evolution of two distinct clades of Beijing and T families of Mycobacterium tuberculosis in Chongqing: a Bayesian population structure and phylogenetic study.Infectious diseases of poverty · 2020Article
- Flavescence Dorée Phytoplasma Has MultipleInternational journal of molecular sciences · 2019Article
- AAA+ Machines of Protein Destruction in Mycobacteria.Frontiers in molecular biosciences · 2017Review
- Comparative Sigma Factor-mRNA Levels in Mycobacterium marinum under Stress Conditions and during Host Infection.PloS one · 2015Article
- Pan-genome analysis of human gastric pathogen H. pylori: comparative genomics and pathogenomics approaches to identify regions associated with pathogenicity and prediction of potential core therapeutic targets.BioMed research international · 2015Article
- Mycobacterium tuberculosis ClpP1 and ClpP2 function together in protein degradation and are required for viability in vitro and during infection.PLoS pathogens · 2012Article
- Mycobacterium tuberculosis ftsZ expression and minimal promoter activity.Tuberculosis (Edinburgh, Scotland) · 2009Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
FtsH is an essential membrane-bound protease that degrades integral membrane proteins as well as cytoplasmic proteins. We show that Mycobacterium tuberculosis (Mtb) ftsH expression levels are upregulated upon exposure to agents that produce reactive oxygen and nitrogen intermediates (ROI and RNI) and growth in macrophages. In partial support of this result is our observation that the Mtb merodiploid overexpressing ftsH shows increased resistance to ROI. ftsH transcript levels are downregulated during stationary phase and starvation. ftsH overexpression strain shows delayed growth and reduced viability in vitro and ex vivo. Finally, we show that the intracellular levels of FtsZ, an essential cell-division protein, are reduced in ftsH-overexpressing strain. Together, our results suggest that Mtb FtsH is a stress-response protein that promotes the pathogen's ability to deal with ROI stress and is possibly involved in the regulation of FtsZ levels.
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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.