Evidence map›Paper›PMID 21884525›Full record

ArticleJournal of neurochemistry2011

Ethanol causes the redistribution of L1 cell adhesion molecule in lipid rafts.

Ningfeng Tang, Benjamin Farah, Min He, Stephanie Fox, Alfred Malouf, Yoav Littner, Cynthia F Bearer

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.4field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 36 citations in OpenAlex.

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  15. Issues in assessing the health risks of n-butanol.Journal of applied toxicology : JAT · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Effect of lipid raft disruption on ethanol inhibition of l1 adhesion.Alcoholism, clinical and experimental research · 2014
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Ningfeng TangDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland 21209, USA.
Benjamin Farah
Min He
Stephanie Fox
Alfred Malouf
Yoav Littner
Cynthia F Bearer
University of Maryland, Baltimore · USCase Western Reserve University · USCleveland Clinic · USDuke-NUS Medical School · SG

Funding

The Role of Lipid Rafts in Fetal Alcohol Spectrum DisorderR01AA016398 · NIAAA · UNIVERSITY OF MARYLAND BALTIMORE · PI BEARER, CYNTHIA FRANCES · 2007 to 2011
$1.5M
NIAAA NIH HHS AA-0 16398NIAAA NIH HHS R01 AA016398
6 · The paper itself

Abstract

Fetal alcohol spectrum disorder is estimated to affect 1% of live births. The similarities between children with fetal alcohol syndrome and those with mutations in the gene encoding L1 cell adhesion molecule (L1) implicates L1 as a target of ethanol developmental neurotoxicity. Ethanol specifically inhibits the neurite outgrowth promoting function of L1 at pharmacologic concentrations. Emerging evidence shows that localized disruption of the lipid rafts reduces L1-mediated neurite outgrowth. We hypothesize that ethanol impairment of the association of L1 with lipid rafts is a mechanism underlying ethanol's inhibition of L1-mediated neurite outgrowth. In this study, we examine the effects of ethanol on the association of L1 and lipid rafts. We show that, in vitro, L1 but not N-cadherin shifts into lipid rafts following treatment with 25 mM ethanol. The ethanol concentrations causing this effect are similar to those inhibiting L1-mediated neurite outgrowth. Increasing chain length of the alcohol demonstrates the same cutoff as that previously shown for inhibition of L1-L1 binding. In addition, in cerebellar granule neurons in which lipid rafts are disrupted with methyl-beta-cyclodextrin, the rate of L1-mediated neurite outgrowth on L1-Fc is reduced to background rate and that this background rate is not ethanol sensitive. These data indicate that ethanol may inhibit L1-mediated neurite outgrowth by retarding L1 trafficking through a lipid raft compartment.

Indexed as

AnimalsAnimals, Newbornbeta-CyclodextrinsButanolsCentral Nervous System DepressantsCerebellumDose-Response Relationship, DrugEthanolMembrane MicrodomainsNeural Cell Adhesion Molecule L1NeuritesNeuronsProtein TransportRatsRats, Sprague-DawleyTime Factorsbeta-CyclodextrinsButanolsCentral Nervous System DepressantsEthanolmethyl-beta-cyclodextrinNeural Cell Adhesion Molecule L1Tubulin

Identifiers

PMID21884525
PMCPMC3221000
OpenAlexW1567716376

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.