ArticlePloS one2009
Phosphatase-dependent regulation of epithelial mitogen-activated protein kinase responses to toxin-induced membrane pores.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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
24 citing papers in PubMed, 38 citations in OpenAlex.
- Crosstalk of MAP3K1 and EGFR signaling mediates gene-environment interactions that block developmental tissue closure.The Journal of biological chemistry · 2024Article
- The Yin and Yang of Pneumolysin During Pneumococcal Infection.Frontiers in immunology · 2022Review
- Panorama of the Intracellular Molecular Concert Orchestrated by Actinoporins, Pore-Forming Toxins from Sea Anemones.Toxins · 2021Review
- Interaction of Macrophages and Cholesterol-Dependent Cytolysins: The Impact on Immune Response and Cellular Survival.Toxins · 2020Review
- Mechanisms protecting host cells against bacterial pore-forming toxins.Cellular and molecular life sciences : CMLS · 2019Review
- Listeriolysin O: A phagosome-specific cytolysin revisited.Cellular microbiology · 2019Review
- Global Proteomic Response ofFrontiers in cellular and infection microbiology · 2019Article
- Cholesterol-Dependent Cytolysins Produced by Vaginal Bacteria: Certainties and Controversies.Frontiers in cellular and infection microbiology · 2019Review
- Phosphokinome Analysis of Barth Syndrome Lymphoblasts Identify Novel Targets in the Pathophysiology of the Disease.International journal of molecular sciences · 2018Article
- c-Jun Proto-Oncoprotein Plays a Protective Role in Lung Epithelial Cells Exposed to Staphylococcal α-Toxin.Frontiers in cellular and infection microbiology · 2018Article
- Biophysical and biochemical strategies to understand membrane binding and pore formation by sticholysins, pore-forming proteins from a sea anemone.Biophysical reviews · 2017Review
- Fusarochromanone-induced reactive oxygen species results in activation of JNK cascade and cell death by inhibiting protein phosphatases 2A and 5.Oncotarget · 2015Article
- Protective role of the dynamin inhibitor Dynasore against the cholesterol-dependent cytolysin of Trueperella pyogenes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Rational manipulation of mRNA folding free energy allows rheostat control of pneumolysin production by Streptococcus pneumoniae.PloS one · 2015Article
- Identification of the ZAK-MKK4-JNK-TGFβ signaling pathway as a molecular target for novel synthetic iminoquinone anticancer compound BA-TPQ.Current cancer drug targets · 2013Article
- Role of pore-forming toxins in bacterial infectious diseases.Microbiology and molecular biology reviews : MMBR · 2013Review
- Overview of community-acquired pneumonia and the role of inflammatory mechanisms in the immunopathogenesis of severe pneumococcal disease.Mediators of inflammation · 2013Review
- Co-infection subverts mucosal immunity in the upper respiratory tract.Current opinion in immunology · 2012Review
- Arcanolysin is a cholesterol-dependent cytolysin of the human pathogen Arcanobacterium haemolyticum.BMC microbiology · 2011Article
- Global functional analyses of cellular responses to pore-forming toxins.PLoS pathogens · 2011Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Diverse bacterial species produce pore-forming toxins (PFT) that can puncture eukaryotic cell membranes. Host cells respond to sublytic concentrations of PFT through conserved intracellular signaling pathways, including activation of mitogen-activated protein kinases (MAPK), which are critical to cell survival. Here we demonstrate that in respiratory epithelial cells p38 and JNK MAPK were phosphorylated within 30 min of exposure to pneumolysin, the PFT from Streptococcus pneumoniae. This activation was tightly regulated, and dephosphorylation of both MAPK occurred within 60 min following exposure. Pretreatment of epithelial cells with inhibitors of cellular phosphatases, including sodium orthovanadate, calyculin A, and okadaic acid, prolonged and intensified MAPK activation. Specific inhibition of MAPK phosphatase-1 did not affect the kinetics of MAPK activation in PFT-exposed epithelial cells, but siRNA-mediated knockdown of serine/threonine phosphatases PP1 and PP2A were potent inhibitors of MAPK dephosphorylation. These results indicate an important role for PP1 and PP2A in termination of epithelial responses to PFT and only a minor contribution of dual-specificity phosphatases, such as MAPK phosphatase-1, which are the major regulators of MAPK signals in other cell types. Epithelial regulation of MAPK signaling in response to membrane disruption involves distinct pathways and may require different strategies for therapeutic interventions.
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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.