ArticleAlcoholism, clinical and experimental research2013
L1 cell adhesion molecule signaling is inhibited by ethanol in vivo.
Article in Alcoholism, clinical and experimental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Recent breakthroughs in understanding the cerebellum's role in fetal alcohol spectrum disorder: A systematic review.Alcohol (Fayetteville, N.Y.) · 2024Pooled it
- White matter abnormalities in fetal alcohol spectrum disorders: Focus on axon growth and guidance.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Altering Cell-Cell Interaction in Prenatal Alcohol Exposure Models: Insight on Cell-Adhesion Molecules During Brain Development.Frontiers in molecular neuroscience · 2021Review
- Choline ameliorates ethanol induced alterations in tyrosine phosphorylation and distribution in detergent-resistant membrane microdomains of L1 cell adhesion molecule in vivo.Birth defects research · 2020Article
- Murine Models for the Study of Fetal Alcohol Spectrum Disorders: An Overview.Frontiers in pediatrics · 2020Review
- Effects of Ethanol on Brain Extracellular Matrix: Implications for Alcohol Use Disorder.Alcoholism, clinical and experimental research · 2016Review
- Toluene disruption of the functions of L1 cell adhesion molecule at concentrations associated with occupational exposures.Pediatric research · 2016Article
- Ethanol Enhances TGF-β Activity by Recruiting TGF-β Receptors From Intracellular Vesicles/Lipid Rafts/Caveolae to Non-Lipid Raft Microdomains.Journal of cellular biochemistry · 2016Article
- Choline Ameliorates Deficits in Balance Caused by Acute Neonatal Ethanol Exposure.Cerebellum (London, England) · 2015Article
- Choline partially prevents the impact of ethanol on the lipid raft dependent functions of l1 cell adhesion molecule.Alcoholism, clinical and experimental research · 2014Article
- Chlorhexidine inhibits L1 cell adhesion molecule-mediated neurite outgrowth in vitro.Pediatric research · 2014Article
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Authors and funding
4 authors.
Funding
Abstract
backgroundFetal alcohol spectrum disorder is an immense public health problem. In vitro studies support the hypothesis that L1 cell adhesion molecule (L1) is a target for ethanol (EtOH) developmental neurotoxicity. L1 is critical for the development of the central nervous system. It functions through signal transduction leading to phosphorylation and dephosphorylation of tyrosines on its cytoplasmic domain. The function of L1 is also dependent on trafficking through lipid rafts (LRs). Our hypothesis is that L1 is a target for EtOH neurotoxicity in vivo. Our objective is to demonstrate changes in L1 phosphorylation/dephosphorylation and LR association in vivo.
methodsRat pups on postnatal day 6 are administered 4.5, 5.25, and 6 g/kg of EtOH divided into 2 doses 2 hours apart, then killed. Cerebella are rapidly frozen for assay. Blood is analyzed for blood EtOH concentration. L1 tyrosine phosphorylation is determined by immunoprecipitation and dephosphorylation of tyrosine 1176 determined by immunoblot. LRs are isolated by sucrose density gradient, and the distribution of L1 in LRs is determined.
resultsEtOH at all doses reduced the relative amount of Y1176 dephosphorylation as well as the relative amount of L1 phosphorylated on other tyrosines. The proportion of L1 present in LRs is significantly increased in pups who received 6 g/kg EtOH compared to intubated controls.
conclusionsL1 is a target for EtOH developmental neurotoxicity in vivo.
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