ArticleJournal of neurochemistry2014
CaMKII represses transcriptionally active β-catenin to mediate acute ethanol neurodegeneration and can phosphorylate β-catenin.
Article in Journal of neurochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
- Molecular Networks of Redox Dysregulation in Fetal Alcohol Spectrum Disorders: Mechanisms and Therapeutic Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- WNT11 Promotes immune evasion and resistance to Anti-PD-1 therapy in liver metastasis.Nature communications · 2025Article
- An overview of current advances in perinatal alcohol exposure and pathogenesis of fetal alcohol spectrum disorders.Journal of neurodevelopmental disorders · 2024Review
- Alcohol exposure suppresses ribosome biogenesis and causes nucleolar stress in cranial neural crest cells.PloS one · 2024Article
- Neural crest cells and fetal alcohol spectrum disorders: Mechanisms and potential targets for prevention.Pharmacological research · 2023Review
- Article
- Assessing CaMPARI as new approach methodology for evaluating neurotoxicity.Neurotoxicology · 2023Article
- Zebrafish Model of Stickler Syndrome Suggests a Role for Col2a1a in the Neural Crest during Early Eye Development.Journal of developmental biology · 2022Article
- The Role of E3 Ligase Pirh2 in Disease.Cells · 2022Review
- Toxic and Teratogenic Effects of Prenatal Alcohol Exposure on Fetal Development, Adolescence, and Adulthood.International journal of molecular sciences · 2021Review
- Epigenetic Modulation of SPCA2 Reverses Epithelial to Mesenchymal Transition in Breast Cancer Cells.Cancers · 2021Article
- From the Farm to the Lab: How Chicken Embryos Contribute to the Field of Teratology.Frontiers in genetics · 2021Review
- Region-dependent regulation of acute ethanol on γ oscillation in the rat hippocampal slices.Psychopharmacology · 2020Article
- Non-canonical WNT5a regulates Epithelial-to-Mesenchymal Transition in the mouse ovarian surface epithelium.Scientific reports · 2020Article
- Postnatal Ethanol-Induced Neurodegeneration Involves CB1R-Mediated β-Catenin Degradation in Neonatal Mice.Brain sciences · 2020Article
- Maternal iron nutriture modulates placental development in a rat model of fetal alcohol spectrum disorder.Alcohol (Fayetteville, N.Y.) · 2020Article
- Alcohol-mediated calcium signals dysregulate pro-survival Snai2/PUMA/Bcl2 networks to promote p53-mediated apoptosis in avian neural crest progenitors.Birth defects research · 2019Article
- Exon level machine learning analyses elucidate novel candidate miRNA targets in an avian model of fetal alcohol spectrum disorder.PLoS computational biology · 2019Article
- Endothelial loss of Fzd5 stimulates PKC/Ets1-mediated transcription of Angpt2 and Flt1.Angiogenesis · 2018Article
- The avian embryo as a model for fetal alcohol spectrum disorder.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2018Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Prenatal ethanol exposure causes persistent neurodevelopmental deficits by inducing apoptosis within neuronal progenitors including the neural crest. The cellular signaling events underlying this apoptosis are unclear. Using an established chick embryo model, we previously identified ethanol's activation of calmodulin-dependent protein kinase II (CaMKII) as a crucial early step in this pathway. Here, we report that CaMKII is pro-apoptotic because it mediates the loss of transcriptionally active β-catenin, which normally provides trophic support to these cells. β-catenin over-expression normalized cell survival in ethanol's presence. CaMKII inhibition similarly restored β-catenin content and transcriptional activity within ethanol-treated cells and prevented their cell death. In contrast, inhibition of alternative effectors known to destabilize β-catenin, including glycogen synthase kinase-3β, Protein Kinase C, JNK, and calpain, failed to normalize cell survival and β-catenin activity in ethanol's presence. Importantly, we found that purified CaMKII can directly phosphorylate β-catenin. Using targeted mutagenesis we identified CaMKII phosphorylation sites within human β-catenin at T332, T472, and S552. This is the first demonstration that β-catenin is a phosphorylation target of CaMKII and represents a novel mechanism by which calcium signals could regulate β-catenin-dependent transcription. These results inform ethanol's neurotoxicity and offer unexpected insights into other neurodevelopmental and neurodegenerative disorders having dysregulated calcium or β-catenin signaling.
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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.