Antagonists of alcohol inhibition of cell adhesion.

@article{Wilkemeyer2000AntagonistsOA,
  title={Antagonists of alcohol inhibition of cell adhesion.},
  author={Michael F. Wilkemeyer and A B Sebastian and S. A. Smith and Michael E. Charness},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2000},
  volume={97 7},
  pages={
          3690-5
        }
}
Increasing evidence suggests that alcohols act within specific binding pockets of selective neural proteins; however, antagonists at these sites have not been identified. 1-Alcohols from methanol through 1-butanol inhibit with increasing potency the cell-cell adhesion mediated by the immunoglobulin cell adhesion molecule L1. An abrupt cutoff exists after 1-butanol, with 1-pentanol and higher 1-alcohols showing no effect. Here, we demonstrate surprisingly strict structural requirements for… Expand
Novel antagonists of alcohol inhibition of l1-mediated cell adhesion: multiple mechanisms of action.
TLDR
It is suggested that selective straight, branched, and cyclic alcohols may act at multiple, discrete sites to antagonize the actions of ethanol and 1-butanol on L1-mediated cell-cell adhesion. Expand
Peptide Antagonists of Ethanol Inhibition of L1-Mediated Cell-Cell Adhesion
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Two structurally unrelated classes of compounds, alcohols and small polypeptides, share two common actions: antagonism of ethanol inhibition of L1-mediated cell adhesion and prevention of ethanol teratogenesis. Expand
Mitogen-activated protein kinase modulates ethanol inhibition of cell adhesion mediated by the L1 neural cell adhesion molecule
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The data suggest that ERK2 phosphorylation of S1248 modulates ethanol inhibition of L1 adhesion by inside-out signaling and that differential regulation of ERK 2 signaling might contribute to genetic susceptibility to FASD. Expand
Ethanol Antagonist Peptides: Structural Specificity without Stereospecificity
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d-NAP, a peptide composed entirely of d-amino acids, was an effective ethanol antagonist in NIH/3T3 cells transfected with human L1 and in the NG108-15 neural cell line, and interestingly, Ala-substituted derivatives of d -NAP demonstrate the same structure-activity relation as the corresponding derivatives of l-N AP. Expand
An alcohol binding site on the neural cell adhesion molecule L1
TLDR
Characterization of alcohol agonist and antagonist binding sites on L1 will aid in understanding the molecular basis for FASD and might accelerate the development of ethanol antagonists. Expand
Ethanol inhibits L1 cell adhesion molecule activation of mitogen‐activated protein kinases
TLDR
It is concluded that ethanol disrupts the signaling pathway between L1 clustering and ERK1/2 activation, and that this occurs independently of the FGFR1 pathway in cerebellar granule cells. Expand
Two Alcohol Binding Residues Interact across a Domain Interface of the L1 Neural Cell Adhesion Molecule and Regulate Cell Adhesion*
TLDR
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. Expand
Neuroprotective Peptide NAPVSIPQ Antagonizes Ethanol Inhibition of L1 Adhesion by Promoting the Dissociation of L1 and Ankyrin-G
TLDR
NAP potently antagonizes ethanol inhibition of L1 adhesion by stimulating EphB2 phosphorylation of L 1-Y1229, suggesting that ADNP may mediate synaptic development partly by activating Eph B2. Expand
L1 cell adhesion molecule signal cascades: targets for ethanol developmental neurotoxicity.
  • C. Bearer
  • Biology, Medicine
  • Neurotoxicology
  • 2001
TLDR
Physiologic concentrations of ethanol have been shown to inhibit L1 mediated neurite outgrowth in cerebellar granule neurons, indicating that L1 and its associated signaling pathways are potentially targets for developmental neurotoxicants. Expand
L1 cell adhesion molecule signaling is inhibited by ethanol in vivo.
TLDR
L1 is a target for EtOH developmental neurotoxicity in vivo, and the proportion of L1 present in LRs is significantly increased in pups who received 6 g/kg EtOH compared to intubated controls. Expand
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