Trichothecene mycotoxins and other protein synthesis inhibitors activate mitogen-activated
protein kinase (MAPKs) via a mechanism that has been termed the “ribotoxic stress …

Trichothecene mycotoxins and other translational inhibitors activate mitogen-activated
protein kinase (MAPKs) by a mechanism called the “ribotoxic stress response,” which drives …

Double-stranded RNA (dsRNA)-activated protein kinase (PKR) is a critical upstream
mediator of the ribotoxic stress response (RSR) to the trichothecene deoxynivalenol (DON) …

Translational inhibitors such as the trichothecene mycotoxin deoxynivalenol (DON) and
ribosomal inhibitory proteins (RIPs) induce mitogen-activated protein kinase (MAPK)–driven …

Trichothecene mycotoxins rapidly induce p38-mediated gene expression and apoptosis in
mononuclear phagocytes via a process known as the ribotoxic stress response. We …

The trichothecene deoxynivalenol (DON) binds to eukaryotic ribosomes and triggers p38-
driven proinflammatory gene expression in the macrophage—a response that is dependent …

The effects of the ribotoxic trichothecene deoxynivalenol (DON) on mitogen-activated protein
kinase (MAPK)-mediated IL-8 expression were investigated in cloned human monocytes …

Ribotoxic Stress Response as a Potential Mechanism for MAP Kinase Activation in Xenobiotic
Toxicity | Toxicological Sciences | Oxford Academic Skip to Main Content Advertisement …

The trichothecene family of mycotoxins inhibit protein synthesis by binding to the ribosomal
peptidyltransferase site. Inhibitors of the peptidyltransferase reaction (eg anisomycin) can …

Deoxynivalenol (DON) and other ribotoxic trichothecenes cause immune stimulation and
suppression in leukocytes by upregulating gene expression and apoptosis, respectively …