ArticleToxicological sciences : an official journal of the Society of Toxicology2008
Double-stranded RNA-activated protein kinase mediates induction of interleukin-8 expression by deoxynivalenol, Shiga toxin 1, and ricin in monocytes.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 56 citations in OpenAlex.
- Gut ribotoxic stress responses facilitate dyslipidemia via metabolic reprogramming: an environmental health prediction.Theranostics · 2024Article
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- Tumor-derived IFN triggers chronic pathway agonism and sensitivity to ADAR loss.Nature medicine · 2019Article
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- The Type II Secretion System of Legionella pneumophila Dampens the MyD88 and Toll-Like Receptor 2 Signaling Pathway in Infected Human Macrophages.Infection and immunity · 2017Article
- Design and synthesis of novel protein kinase R (PKR) inhibitors.Molecular diversity · 2016Article
- Article
- Ribosomal alteration-derived signals for cytokine induction in mucosal and systemic inflammation: noncanonical pathways by ribosomal inactivation.Mediators of inflammation · 2014Review
- Targeting ricin to the ribosome.Toxicon : official journal of the International Society on Toxinology · 2013Review
- Activation of host mitogen-activated protein kinases by secreted Legionella pneumophila effectors that inhibit host protein translation.Infection and immunity · 2012Article
- Regulation of cytokine and chemokine expression by the ribotoxic stress response elicited by Shiga toxin type 1 in human macrophage-like THP-1 cells.Infection and immunity · 2012Article
- The double-stranded RNA bluetongue virus induces type I interferon in plasmacytoid dendritic cells via a MYD88-dependent TLR7/8-independent signaling pathway.Journal of virology · 2012Article
- Activation of cell stress response pathways by Shiga toxins.Cellular microbiology · 2012Review
- Ricin and Shiga toxins: effects on host cell signal transduction.Current topics in microbiology and immunology · 2012Review
- Shiga toxins induce autophagy leading to differential signalling pathways in toxin-sensitive and toxin-resistant human cells.Cellular microbiology · 2011Article
- Deoxynivalenol-induced proinflammatory gene expression: mechanisms and pathological sequelae.Toxins · 2010Review
- Hematopoietic cell kinase associates with the 40S ribosomal subunit and mediates the ribotoxic stress response to deoxynivalenol in mononuclear phagocytes.Toxicological sciences : an official journal of the Society of Toxicology · 2010Article
- Satratoxin G interaction with 40S and 60S ribosomal subunits precedes apoptosis in the macrophage.Toxicology and applied pharmacology · 2009Article
- Activation of the cholinergic antiinflammatory pathway reduces ricin-induced mortality and organ failure in mice.Molecular medicine (Cambridge, Mass.)Article
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Authors and funding
5 authors at 4 institutions in 4 countries.
Funding
Abstract
Translational inhibitors such as the trichothecene mycotoxin deoxynivalenol (DON) and ribosomal inhibitory proteins (RIPs) induce mitogen-activated protein kinase (MAPK)-driven chemokine and cytokine production by a mechanism known as the ribotoxic stress response (RSR). Double-stranded RNA-activated protein kinase (PKR) associates with the ribosome making it uniquely positioned to sense 28S ribosomal RNA damage and initiate the RSR. We have previously shown that PKR mediates DON-induced MAPK phosphorylation in macrophages and monocytes. The purpose of this study was to test the hypothesis that PKR is essential for induction of interleukin (IL)-8 expression in monocytes by DON and two prototypical RIPs, ricin, and Shiga toxin 1 (Stx1). Preincubation of human monocytic U937 cells with the PKR inhibitors C16 and 2-aminopurine (2-AP) blocked DON-induced expression of IL-8 protein and mRNA. Induction of IL-8 expression was similarly impaired in U937 cells stably transfected with a dominant negative PKR plasmid (UK9M) as compared with cells transfected with control plasmid (UK9C). Nuclear factor-kappa B binding, which has been previously shown to be a requisite for DON-induced IL-8 transcription, was markedly reduced in UK9M cells as compared with UK9C cells. As observed for DON, ricin-, and Stx1-induced IL-8 expression was suppressed by the PKR inhibitors C16 and 2-AP as well as impaired in UK9M cells. Taken together, these data indicate that PKR plays a common role in IL-8 induction by DON and the two RIPs, suggesting that this kinase might be a critical factor in RSR.
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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.