ArticleThe Journal of biological chemistry2012
A universally conserved ATPase regulates the oxidative stress response in Escherichia coli.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- The unconventional G protein AtYchF1 interacts with ribosomal protein AtRPS7 to modulate selective translation for balancing plant growth and stress responses in Arabidopsis.Plant communications · 2026Article
- A Mechanistic Model of Cry2Ab12 Toxicity AgainstToxins · 2026Article
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- Menthol's disruptive effects on kanamycin-resistant Escherichia coli energy metabolism and ion fluxes.Biophysical reports · 2025Article
- Conserved GTPase OLA1 promotes efficient translation on D/E-rich mRNA.Nature communications · 2025Article
- Development of a Recombinase-Mediated Cassette Exchange System for Gene Knockout and Expression of Non-Native Gene Sequences inVaccines · 2025Article
- Novel antibiotics againstMedComm · 2025Article
- The master regulator OxyR orchestrates bacterial oxidative stress response genes in space and time.Cell systems · 2024Article
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- Article
- The Universally Conserved Unconventional G Protein YchF Is Critical for Growth and Stress Response.Life (Basel, Switzerland) · 2023Review
- OLA1 Phosphorylation Governs the Mitochondrial Bioenergetic Function of Pulmonary Vascular Cells.American journal of respiratory cell and molecular biology · 2023Article
- At the Crossroad of Nucleotide Dynamics and Protein Synthesis in Bacteria.Microbiology and molecular biology reviews : MMBR · 2023Review
- Physiological roles of catalases Cat1 and Cat2 in Myxococcus xanthus.Journal of microbiology (Seoul, Korea) · 2022Article
- OLA-1, an Obg-like ATPase, integrates hunger with temperature information in sensory neurons in C. elegans.PLoS genetics · 2022Article
- The Role of the Universally Conserved ATPase YchF/Ola1 in Translation Regulation during Cellular Stress.Microorganisms · 2021Review
- The CopA2-Type PFrontiers in microbiology · 2021Article
- The Universally Conserved ATPase YchF Regulates Translation of Leaderless mRNA in Response to Stress Conditions.Frontiers in molecular biosciences · 2021Article
- Article
- Resistance to oxidative stress by inner membrane protein ElaB is regulated by OxyR and RpoS.Microbial biotechnology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
YchF is an evolutionarily conserved ATPase of unknown function. In humans, the YchF homologue hOla1 appears to influence cell proliferation and was found to be up-regulated in many tumors. A possible involvement in regulating the oxidative stress response was also suggested, but details on the underlying mechanism are lacking. For gaining insight into YchF function, we used Escherichia coli as a model organism and found that YchF overexpression resulted in H(2)O(2) hypersensitivity. This was not caused by transcriptional or translational down-regulation of H(2)O(2)-scavenging enzymes. Instead, we observed YchF-dependent inhibition of catalase activity and a direct interaction with the major E. coli catalase KatG. KatG inhibition was dependent on the ATPase activity of YchF and was regulated by post-translational modifications, most likely including an H(2)O(2)-dependent dephosphorylation. We furthermore showed that YchF expression is repressed by the transcription factor OxyR and further post-translationally modified in response to H(2)O(2). In summary, our data show that YchF functions as a novel negative regulator of the oxidative stress response in E. coli. Considering the available data on hOla1, YchF/Ola1 most likely execute similar functions in bacteria and humans, and their up-regulation inhibits the ability of the cells to scavenge damaging reactive oxygen species.
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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.