ReviewSmall GTPases2015
Switching Rho GTPase activation into effective antibacterial defenses requires the caspase-1/IL-1beta signaling axis.
Review in Small GTPases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Review
- Differential interleukin-1β induction by uropathogenic Escherichia coli correlates with its phylotype and serum C-reactive protein levels in Korean infants.Scientific reports · 2019Article
- The Bacterial Toxin CNF1 Induces Activation and Maturation of Human Monocyte-Derived Dendritic Cells.International journal of molecular sciences · 2018Article
- Small-Volume Flow Cytometry-Based Multiplex Analysis of the Activity of Small GTPases.Methods in molecular biology (Clifton, N.J.) · 2018Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The monitoring of the activation state of Rho GTPases has emerged as a potent innate immune mechanism for detecting pathogens. In the March issue of PLOS Pathogens, we show that the activation of Rho GTPases by the CNF1 toxin during E. coli-triggered bacteremia leads to a GR1(+)cell-mediated efficient bacterial clearing and improves host survival. Host alarm requires the Caspase-1/IL-1beta signaling axis. Furthermore, we discover that pathogenic bacteria have the capacity to block immune responses via the expression of the α-hemolysin pore-forming toxin. In this commentary, we will comment on these findings and highlight the questions raised by this example of attack-defense mechanisms used alternatively by the pathogen and the host during blood infection.
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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.