ArticleProceedings of the National Academy of Sciences of the United States of America2003
Differential effects of ethanol antagonism and neuroprotection in peptide fragment NAPVSIPQ prevention of ethanol-induced developmental toxicity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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45 citing papers in PubMed, 112 citations in OpenAlex.
- The Role of the Immunoglobulin Superfamily of Cell Adhesion Molecules in Intellectual Disability.Cells · 2026Review
- Neural crest cells and fetal alcohol spectrum disorders: Mechanisms and potential targets for prevention.Pharmacological research · 2023Review
- Fetal alcohol spectrum disorders.Nature reviews. Disease primers · 2023Review
- Fetal Alcohol Spectrum Disorders: Awareness to Insight in Just 50 Years.Alcohol research : current reviews · 2022Article
- Neuroprotective Peptide NAPVSIPQ Antagonizes Ethanol Inhibition of L1 Adhesion by Promoting the Dissociation of L1 and Ankyrin-G.Biological psychiatry · 2020Article
- Reduction of aluminum ion neurotoxicity through a small peptide application - NAP treatment of Alzheimer's disease.Journal of food and drug analysis · 2019Article
- A Novel Peptide Restricts Ethanol Modulation of the BK Channel In Vitro and In Vivo.The Journal of pharmacology and experimental therapeutics · 2018Article
- Effects of prenatal alcohol exposure (PAE): insights into FASD using mouse models of PAE.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2018Review
- 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
- ADNP, a Microtubule Interacting Protein, Provides Neuroprotection Through End Binding Proteins and Tau: An Amplifier Effect.Frontiers in molecular neuroscience · 2018Article
- Microtubule stabilising peptides rescue tau phenotypes in-vivo.Scientific reports · 2016Article
- Sexual divergence in microtubule function: the novel intranasal microtubule targeting SKIP normalizes axonal transport and enhances memory.Molecular psychiatry · 2016Article
- D-SAL and NAP: Two Peptides Sharing a SIP Domain.Journal of molecular neuroscience : MN · 2016Article
- Proceedings of the 2015 Annual Meeting of the Fetal Alcohol Spectrum Disorders Study Group.Alcohol (Fayetteville, N.Y.) · 2016Article
- Microtubule-Tau Interaction as a Therapeutic Target for Alzheimer's Disease.Journal of molecular neuroscience : MN · 2016Review
- Effect of lipid raft disruption on ethanol inhibition of l1 adhesion.Alcoholism, clinical and experimental research · 2014Article
- The NAP motif of activity-dependent neuroprotective protein (ADNP) regulates dendritic spines through microtubule end binding proteins.Molecular psychiatry · 2014Article
- Article
- NAP alpha-aminoisobutyric acid (IsoNAP).Journal of molecular neuroscience : MN · 2014Article
- 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
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6 authors at 1 institution in 1 country.
Funding
Abstract
NAPVSIPQ (NAP), an active fragment of the glial-derived activity-dependent neuroprotective protein, is protective at femtomolar concentrations against a wide array of neural insults and prevents ethanol-induced fetal wastage and growth retardation in mice. NAP also antagonizes ethanol inhibition of L1-mediated cell adhesion (ethanol antagonism). We performed an Ala scanning substitution of NAP to determine the role of ethanol antagonism and neuroprotection in NAP prevention of ethanol embryotoxicity. The Ser-Ile-Pro region of NAP was crucial for both ethanol antagonism and protection of cortical neurons from tetrodotoxin toxicity (neuroprotection). Ala replacement of either Ser-5 or Pro-7 (P7A-NAP) abolished NAP neuroprotection but minimally changed the efficacy of NAP ethanol antagonism. In contrast, Ala replacement of Ile-6 (I6A-NAP) caused a decrease in potency (>2 logarithmic orders) with only a small reduction (<10%) in the efficacy of NAP neuroprotection but markedly reduced the efficacy (50%) and the potency (5 logarithmic orders) of NAP ethanol antagonism. Ethanol significantly reduced the number of paired somites in mouse whole-embryo culture; this effect was prevented significantly by 100 pM NAP or by 100 pM P7A-NAP, but not by 100 pM I6A-NAP. The structure-activity relation for NAP prevention of ethanol embryotoxicity was similar to that for NAP ethanol antagonism and different from that for NAP neuroprotection. These findings support the hypothesis that NAP antagonism of ethanol inhibition of L1 adhesion plays a central role in NAP prevention of ethanol embryotoxicity and highlight the potential importance of ethanol effects on L1 in the pathophysiology of fetal alcohol syndrome.
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