ArticleCerebellum (London, England)2015
Deficient PKR in RAX/PKR Association Ameliorates Ethanol-Induced Neurotoxicity in the Developing Cerebellum.
Article in Cerebellum (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Recent breakthroughs in understanding the cerebellum's role in fetal alcohol spectrum disorder: A systematic review.Alcohol (Fayetteville, N.Y.) · 2024Pooled it
- Review
- Unravelling the role of protein kinase R (PKR) in neurodegenerative disease: a review.Molecular biology reports · 2025Review
- Assessment of ethanol exposure from hand sanitizer use and potential for developmental toxicity in nursing infants.Journal of applied toxicology : JAT · 2022Review
- The Potential Role of Protein Kinase R as a Regulator of Age-Related Neurodegeneration.Frontiers in aging neuroscience · 2021Review
- 4-Phenylbutyric Acid Protects Against Ethanol-Induced Damage in the Developing Mouse Brain.Alcoholism, clinical and experimental research · 2019Article
- Ethanol-Induced Neurodegeneration and Glial Activation in the Developing Brain.Brain sciences · 2016Review
- Endoplasmic Reticulum Stress and Ethanol Neurotoxicity.Biomolecules · 2015Review
- Exposure of neonatal rats to alcohol has differential effects on neuroinflammation and neuronal survival in the cerebellum and hippocampus.Journal of neuroinflammation · 2015Article
- Effects of Ethanol on the Cerebellum: Advances and Prospects.Cerebellum (London, England) · 2015Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Ethanol-induced neuronal loss is closely related to the pathogenesis of fetal alcohol spectrum disorders. The cerebellum is one of the brain areas that are most sensitive to ethanol. The mechanism underlying ethanol neurotoxicity remains unclear. Our previous in vitro studies have shown that the double-stranded RNA (dsRNA)-activated protein kinase (PKR) regulates neuronal apoptosis upon ethanol exposure and ethanol activates PKR through association with its intracellular activator RAX. However, the role of PKR and its interaction with RAX in vivo have not been investigated. In the current study, by utilizing N-PKR-/- mice, C57BL/6J mice with a deficient RAX-binding domain in PKR, we determined the critical role of RAX/PKR association in PKR-regulated ethanol neurotoxicity in the developing cerebellum. Our data indicate that while N-PKR-/- mice have a similar BAC profile as wild-type mice, ethanol induces less brain/body mass reduction as well as cerebellar neuronal loss. In addition, ethanol promotes interleukin-1β (IL-1β) secretion, and IL-1β is a master cytokine regulating inflammatory response. Importantly, ethanol-promoted IL-1β secretion is inhibited in the developing cerebellum of N-PKR-/- mice. Thus, RAX/PKR interaction and PKR activation regulate ethanol neurotoxicity in the developing cerebellum, which may involve ethanol-induced neuroinflammation. Further, PKR could be a possible target for pharmacological intervention to prevent or treat fetal alcohol spectrum disorder (FASD).
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Registered trials
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