ArticleThe Journal of biological chemistry2011
Two alcohol binding residues interact across a domain interface of the L1 neural cell adhesion molecule and regulate cell adhesion.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Integrated Network and Transcriptomic Analyses Identify a Candidate Ethanol-ADAM17 Molecular Axis Associated with Glioblastoma Progression.International journal of molecular sciences · 2026Article
- Clinical Diagnosis and Management of Fetal Alcohol Spectrum Disorder and Sensory Processing Disorder in Children.Children (Basel, Switzerland) · 2024Review
- 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
- 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
- Titrating Tipsy Targets: The Neurobiology of Low-Dose Alcohol.Trends in pharmacological sciences · 2017Review
- Effect of lipid raft disruption on ethanol inhibition of l1 adhesion.Alcoholism, clinical and experimental research · 2014Article
- Connecting teratogen-induced congenital heart defects to neural crest cells and their effect on cardiac function.Birth defects research. Part C, Embryo today : reviews · 2014Review
- Mitogen-activated protein kinase modulates ethanol inhibition of cell adhesion mediated by the L1 neural cell adhesion molecule.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- L1 cell adhesion molecule signaling is inhibited by ethanol in vivo.Alcoholism, clinical and experimental research · 2013Article
- L1CAM and its cell-surface mutants: new mechanisms and effects relevant to the physiology and pathology of neural cells.Journal of neurochemistry · 2013Article
- Taok2 controls behavioral response to ethanol in mice.Genes, brain, and behavior · 2013Article
- Homophilic interaction of the L1 family of cell adhesion molecules.Experimental & molecular medicine · 2012Review
- Effects of ethanol and NAP on cerebellar expression of the neural cell adhesion molecule L1.PloS one · 2011Article
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Authors and funding
5 authors at 3 institutions in 1 country.
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Abstract
Ethanol may cause fetal alcohol spectrum disorders (FASD) in part by inhibiting cell adhesion mediated by the L1 neural cell adhesion molecule. Azialcohols photolabel Glu-33 and Tyr-418, two residues that are predicted by homology modeling to lie within 2.8 Å of each other at the interface between the Ig1 and Ig4 domains of L1 (Arevalo, E., Shanmugasundararaj, S., Wilkemeyer, M. F., Dou, X., Chen, S., Charness, M. E., and Miller, K. W. (2008) Proc. Natl. Acad. Sci. U.S.A. 105, 371-375). Using transient transfection of NIH/3T3 cells with wild type (WT-L1) and mutated L1, we found that cysteine substitution of both residues (E33C/Y418C-L1) significantly increased L1 adhesion above levels observed for WT-L1 or the single cysteine substitutions E33C-L1 or Y418C-L1. The reducing agent β-mercaptoethanol (βME) reversibly decreased the adhesion of E33C/Y418C-L1, but had no effect on WT-L1, E33C-L1, or Y418C-L1. Thus, disulfide bond formation occurs between Cys-33 and Cys-418, confirming both the close proximity of these residues and the importance of Ig1-Ig4 interactions in L1 adhesion. Maximal ethanol inhibition of cell adhesion was significantly lower in cells expressing E33C/Y418C-L1 than in those expressing WT-L1, E33C-L1, or Y418C-L1. Moreover, the effects of βME and ethanol on E33C/Y418C-L1 adhesion were non-additive. The cutoff for alcohol inhibition of WT-L1 adhesion was between 1-butanol and 1-pentanol. Increasing the size of the alcohol binding pocket by mutating Glu-33 to Ala-33, increased the alcohol cutoff from 1-butanol to 1-decanol. These findings support the hypothesis that alcohol binding within a pocket bordered by Glu-33 and Tyr-418 inhibits L1 adhesion by disrupting the Ig1-Ig4 interaction.
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