Ethanol Antagonist Peptides: Structural Specificity without Stereospecificity

@article{Wilkemeyer2004EthanolAP,
  title={Ethanol Antagonist Peptides: Structural Specificity without Stereospecificity},
  author={Michael F. Wilkemeyer and Shao-Yu Chen and Carrie E Menkari and Kathleen K. Sulik and Michael E. Charness},
  journal={Journal of Pharmacology and Experimental Therapeutics},
  year={2004},
  volume={309},
  pages={1183 - 1189}
}
Increasing evidence suggests that ethanol damages the developing nervous system partly by disrupting the L1 cell adhesion molecule. Ethanol inhibits L1-mediated cell adhesion, and compounds that antagonize this action also prevent ethanol-induced embryotoxicity. Two such compounds are the small peptides NAPVSIPQ (NAP) and SALLRSIPA (SAL). We showed previously that NAP and SAL antagonize ethanol inhibition of L1 adhesion at femtomolar to picomolar concentrations. Here we demonstrate that… 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
Synergistic effects of the peptide fragment D-NAPVSIPQ on ethanol inhibition of synaptic plasticity and NMDA receptors in rat hippocampus
TLDR
The findings suggest that D-NAP and 1-octanol selectively interact with NMDA receptors in an ethanol-dependent manner, further implicating the L1 cell adhesion molecule in alcohol-related brain disorders. Expand
Peptide-Mediated Protection from Ethanol-Induced Neural Tube Defects
TLDR
The ability of NAP and SAL to prevent ethanol-induced NTDs is demonstrated and the hypothesis that ethanol teratogenesis is caused in part by ethanol inhibition of L1-mediated cell adhesion is supported. 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
D-SAL and NAP: Two Peptides Sharing a SIP Domain
TLDR
Evaluating the effect of NAP and D-SAL on peripheral neuropathy and cognitive decline in a rat model of diabetes indicated an immediate sensory neuropathy in the diabetic model was prevented by both peptides and a later neuropathic phase, prevented only by NAP treatment. Expand
Effect of Lipid Raft Disruption on Ethanol Inhibition of L1 Adhesion
TLDR
Findings indicate that EtOH does not inhibit L1 adhesion in NIH/3T3 cells by inducing the translocation of L1 into lipid rafts. Expand
Concurrent dietary administration of D-SAL and ethanol diminishes ethanol's teratogenesis.
TLDR
It is demonstrated that oral D-SAL can prevent ethanol-induced ocular defects and may also prove valuable in preventinganol-induced brain defects, as well as in preventing teratogenicity in mice. 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
VIP/PACAP-Based Drug Development: The ADNP/NAP-Derived Mirror Peptides SKIP and D-SKIP Exhibit Distinctive in vivo and in silico Effects
TLDR
Previous evidence suggested potential antagonistic features for D-SKIP, compared with the neuroprotective peptide SKIP, as was observed by NMR analysis and social/olfactory functional testing, corroborate the notion of D- SKIP acting as an antagonist, thus distinguishing it from the neuroProtective SKIP. Expand
Neurotrophic Peptides, ADNF-9 and NAP, Prevent Alcohol-Induced Apoptosis at Midgestation in Fetal Brains of C57BL/6 Mouse
TLDR
The results show that NAP and ADNF-9 significantly prevented alcohol-induced weight reduction of fetal brains and may pave the path toward potential therapeutics against alcohol intoxication during pregnancy stages. Expand
...
1
2
3
4
...

References

SHOWING 1-10 OF 45 REFERENCES
Peptide Antagonists of Ethanol Inhibition of L1-Mediated Cell-Cell Adhesion
TLDR
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
Differential effects of ethanol antagonism and neuroprotection in peptide fragment NAPVSIPQ prevention of ethanol-induced developmental toxicity
TLDR
The hypothesis that NAP antagonism of ethanol inhibition of L1 adhesion plays a central role in NAP prevention of ethanol embryotoxicity is supported and the potential importance of ethanol effects on L1 in the pathophysiology of fetal alcohol syndrome is highlighted. Expand
Antagonists of alcohol inhibition of cell adhesion.
TLDR
Notably strict structural requirements for alcohol inhibition of cell-cell adhesion are demonstrated in L1-transfected NIH 3T3 fibroblasts and in NG108-15 neuroblastoma x glioma hybrid cells treated with BMP-7, an inducer of L1 and neural cell adhesion molecule. 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
Designed helical peptides inhibit an intramembrane protease.
TLDR
It is shown that short peptides designed to adopt a helical conformation in solution are inhibitors of gamma-secretase in both cells and enzyme preparations, suggesting a general strategy for the development of potent and specific inhibitors of intramembrane proteases. Expand
A femtomolar-acting neuroprotective peptide.
TLDR
These studies identify a potent neuroprotective glial protein and an active peptide that provide a basis for developing treatments of currently intractable neurodegenerative diseases. Expand
Ethanol inhibits neural cell-cell adhesion.
TLDR
It is shown that concentrations of ethanol achieved during social drinking inhibit hOP-1-induced cell clustering without affecting cell proliferation, the induction and cell surface expression of N-CAM and L1, or the alternative splicing and sialylation of N -CAM. Expand
Achatin-I, an endogenous neuroexcitatory tetrapeptide from Achatina fulica Férussac containing a D-amino acid residue.
A tetrapeptide named achatin-I was purified from the suboesophageal and cerebral ganglia of the African giant snail Achatina fulica Férussac, and evoked a potent neuroexcitatory effect. The aminoExpand
Ethanol Inhibits L1-mediated Neurite Outgrowth in Postnatal Rat Cerebellar Granule Cells*
TLDR
One mechanism of ethanol’s toxicity to the developing central nervous system may be the inhibition of L1-mediated neurite outgrowth, which is similar to those of patients with mutations in L1, a neural cell adhesion molecule. Expand
All-D amino acid-containing channel-forming antibiotic peptides.
TLDR
The D enantiomers of three naturally occurring antibiotics--cecropin A, magainin 2 amide, and melittin--were synthesized and it is suggested that the mode of action of these peptides on the membranes of bacteria, erythrocytes, plasmodia, and artificial lipid bilayers may be similar and involves the formation of ion-channel pores spanning the membranes, but without specific interaction with chiral receptors or enzymes. Expand
...
1
2
3
4
5
...