ArticleProceedings of the National Academy of Sciences of the United States of America2013
Mitogen-activated protein kinase modulates ethanol inhibition of cell adhesion mediated by the L1 neural cell adhesion molecule.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- The Role of the Immunoglobulin Superfamily of Cell Adhesion Molecules in Intellectual Disability.Cells · 2026Review
- Associations of Low-Level Prenatal Alcohol and Cannabis Exposure With Adolescent Cognitive Trajectories.Alcohol, clinical & experimental research · 2026Article
- The Role of the Hedgehog Pathway in Alcohol-Induced Birth Defects.Advances in experimental medicine and biology · 2026Review
- Clinical Diagnosis and Management of Fetal Alcohol Spectrum Disorder and Sensory Processing Disorder in Children.Children (Basel, Switzerland) · 2024Review
- Short-term transcriptomic changes in the mouse neural tube induced by an acute alcohol exposure.Alcohol (Fayetteville, N.Y.) · 2023Article
- Embryonic ethanol exposure disrupts craniofacial neuromuscular integration in zebrafish larvae.Frontiers in physiology · 2023Article
- The pro-apoptotic Bax gene modifies susceptibility to craniofacial dysmorphology following gastrulation-stage alcohol exposure.Birth defects research · 2022Article
- Zebrafish models of fetal alcohol spectrum disorders.Genesis (New York, N.Y. : 2000) · 2021Review
- Loss of tumor protein 53 protects against alcohol-induced facial malformations in mice and zebrafish.Alcoholism, clinical and experimental research · 2021Article
- Transcriptomic analyses of gastrulation-stage mouse embryos with differential susceptibility to alcohol.Disease models & mechanisms · 2021Article
- Altering Cell-Cell Interaction in Prenatal Alcohol Exposure Models: Insight on Cell-Adhesion Molecules During Brain Development.Frontiers in molecular neuroscience · 2021Review
- Neuroprotective Peptide NAPVSIPQ Antagonizes Ethanol Inhibition of L1 Adhesion by Promoting the Dissociation of L1 and Ankyrin-G.Biological psychiatry · 2020Article
- Effects of Acute Alcohol Exposure on Layer 5 Pyramidal Neurons of Juvenile Mice.Cellular and molecular neurobiology · 2018Article
- L1 coupling to ankyrin and the spectrin-actin cytoskeleton modulates ethanol inhibition of L1 adhesion and ethanol teratogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- The enduring impact of neurulation stage alcohol exposure: A combined behavioral and structural neuroimaging study in adult male and female C57BL/6J mice.Behavioural brain research · 2018Article
- Electroacupuncture Restores Locomotor Functions After Mouse Spinal Cord Injury in Correlation With Reduction of PTEN and p53 Expression.Frontiers in molecular neuroscience · 2018Article
- Gene-environment interactions in development and disease.Wiley interdisciplinary reviews. Developmental biology · 2017Review
- The Genetics of Fetal Alcohol Spectrum Disorders.Alcoholism, clinical and experimental research · 2016Review
- Drinking During Pregnancy and the Developing Brain: Is Any Amount Safe?Trends in cognitive sciences · 2016Article
- Proceedings of the 2015 Annual Meeting of the Fetal Alcohol Spectrum Disorders Study Group.Alcohol (Fayetteville, N.Y.) · 2016Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
There is a genetic contribution to fetal alcohol spectrum disorders (FASD), but the identification of candidate genes has been elusive. Ethanol may cause FASD in part by decreasing the adhesion of the developmentally critical L1 cell adhesion molecule through interactions with an alcohol binding pocket on the extracellular domain. Pharmacologic inhibition or genetic knockdown of ERK2 did not alter L1 adhesion, but markedly decreased ethanol inhibition of L1 adhesion in NIH/3T3 cells and NG108-15 cells. Likewise, leucine replacement of S1248, an ERK2 substrate on the L1 cytoplasmic domain, did not decrease L1 adhesion, but abolished ethanol inhibition of L1 adhesion. Stable transfection of NIH/3T3 cells with human L1 resulted in clonal cell lines in which L1 adhesion was consistently sensitive or insensitive to ethanol for more than a decade. ERK2 activity and S1248 phosphorylation were greater in ethanol-sensitive NIH/3T3 clonal cell lines than in their ethanol-insensitive counterparts. Ethanol-insensitive cells became ethanol sensitive after increasing ERK2 activity by transfection with a constitutively active MAP kinase kinase 1. Finally, embryos from two substrains of C57BL mice that differ in susceptibility to ethanol teratogenesis showed corresponding differences in MAPK activity. Our data suggest that ERK2 phosphorylation of S1248 modulates ethanol inhibition of L1 adhesion by inside-out signaling and that differential regulation of ERK2 signaling might contribute to genetic susceptibility to FASD. Moreover, identification of a specific locus that regulates ethanol sensitivity, but not L1 function, might facilitate the rational design of drugs that block ethanol neurotoxicity.
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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.