Loss of cellular K+ mimics ribotoxic stress. Inhibition of protein synthesis and activation of the stress kinases SEK1/MKK4, stress-activated protein kinase/c-Jun NH2-terminal kinase 1, and p38/HOG1 by palytoxin.
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Modulation of translation and induction of autophagy by bacterial exoproductsSuppression of ribosomal function triggers innate immune signaling through activation of the NLRP3 inflammasomePalytoxin and an Ostreopsis toxin extract increase the levels of mRNAs encoding inflammation-related proteins in human macrophages via p38 MAPK and NF-κBInhibition of prefrontal protein synthesis following recall does not disrupt memory for trace fear conditioning.Administration of ricin induces a severe inflammatory response via nonredundant stimulation of ERK, JNK, and P38 MAPK and provides a mouse model of hemolytic uremic syndrome.ZAK is required for doxorubicin, a novel ribotoxic stressor, to induce SAPK activation and apoptosis in HaCaT cells.Modulation of protein kinase signaling cascades by palytoxin.Deoxynivalenol-induced proinflammatory gene expression: mechanisms and pathological sequelae.Palytoxin: exploiting a novel skin tumor promoter to explore signal transduction and carcinogenesis.Head and neck cancer cells and xenografts are very sensitive to palytoxin: decrease of c-jun n-terminale kinase-3 expression enhances palytoxin toxicity.Activation of p38 mitogen-activated protein kinase and c-Jun NH(2)-terminal kinase by double-stranded RNA and encephalomyocarditis virus: involvement of RNase L, protein kinase R, and alternative pathways.Protein expression profiling of mouse thymoma cells upon exposure to the trichothecene deoxynivalenol (DON): implications for its mechanism of action.The UV (Ribotoxic) stress response of human keratinocytes involves the unexpected uncoupling of the Ras-extracellular signal-regulated kinase signaling cascade from the activated epidermal growth factor receptor.A functional variant (-1304T>G) in the MKK4 promoter contributes to a decreased risk of lung cancer by increasing the promoter activity.Requirement for SAPK-JNK signaling in the induction of apoptosis by ribosomal stress in REH lymphoid leukemia cells.The Unexpected Tuners: Are LncRNAs Regulating Host Translation during Infections?Scientific Opinion on marine biotoxins in shellfish - Palytoxin groupUltraviolet radiation triggers the ribotoxic stress response in mammalian cells.Different mechanisms of c-Jun NH(2)-terminal kinase-1 (JNK1) activation by ultraviolet-B radiation and by oxidative stressors.
P2860
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P2860
Loss of cellular K+ mimics ribotoxic stress. Inhibition of protein synthesis and activation of the stress kinases SEK1/MKK4, stress-activated protein kinase/c-Jun NH2-terminal kinase 1, and p38/HOG1 by palytoxin.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年学术文章
@wuu
1998年学术文章
@zh-cn
1998年学术文章
@zh-hans
1998年学术文章
@zh-my
1998年学术文章
@zh-sg
1998年學術文章
@yue
1998年學術文章
@zh
1998年學術文章
@zh-hant
name
Loss of cellular K+ mimics rib ...... 1, and p38/HOG1 by palytoxin.
@en
type
label
Loss of cellular K+ mimics rib ...... 1, and p38/HOG1 by palytoxin.
@en
prefLabel
Loss of cellular K+ mimics rib ...... 1, and p38/HOG1 by palytoxin.
@en
P2860
P356
P1476
Loss of cellular K+ mimics rib ...... 1, and p38/HOG1 by palytoxin.
@en
P2093
P2860
P304
P356
10.1074/JBC.273.6.3528
P407
P577
1998-02-01T00:00:00Z