Evidence map›Paper›PMID 16478533›Full record

ArticleJournal of neurochemistry2006

Ethanol inhibits L1 cell adhesion molecule activation of mitogen-activated protein kinases.

Ningfeng Tang, Min He, Mary Ann O'Riordan, Chloe Farkas, Kevin Buck, Vance Lemmon, Cynthia F Bearer

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of neurochemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
8.2field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. L1 cell adhesion molecule signaling is inhibited by ethanol in vivo.Alcoholism, clinical and experimental research · 2013
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. L1CAM malfunction in the nervous system and human carcinomas.Cellular and molecular life sciences : CMLS · 2010
    Review
  17. Overexpression of serum response factor restores ocular dominance plasticity in a model of fetal alcohol spectrum disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  18. Normal development of brain circuits.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2010
    Review
  19. Article
  20. 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 2 institutions in 1 country.

Ningfeng TangDepartment of Pediatrics, Case Western Reserve University, Cleveland, Ohio, USA.
Min He
Mary Ann O'Riordan
Chloe Farkas
Kevin Buck
Vance Lemmon
Cynthia F Bearer
Case Western Reserve University · USUniversity of Miami · US

Funding

CELL ADHESION MOLECULES IN NERVOUS SYSTEM DEVELOPMENTR01HD039884 · NICHD · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI LEMMON, VANCE P · 2001 to 2005
$1.5M
THE GROWTH OF RETINAL GANGLION CELL AXONSR01EY005285 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LEMMON, VANCE P · 1985 to 2004
$1.4M
ETHANOL AND L1 MEDIATED NEURITE OUTGROWTHR01AA011839 · NIAAA · CASE WESTERN RESERVE UNIVERSITY · PI BEARER, CYNTHIA F. · 1999 to 2003
$1.1M
NEI NIH HHS EY-05285NEI NIH HHS R01 EY005285NIAAA NIH HHS AA-11839NIAAA NIH HHS R01 AA011839NICHD NIH HHS R01 HD039884
6 · The paper itself

Abstract

Inhibition of the functions of L1 cell adhesion molecule (L1) by ethanol has been implicated in the pathogenesis of the neurodevelopmental aspects of the fetal alcohol syndrome (FAS). Ethanol at pharmacological concentrations has been shown to inhibit L1-mediated neurite outgrowth of rat post-natal day 6 cerebellar granule cells (CGN). Extracellular signal-related kinases (ERK) 1/2 activation occurs following L1 clustering. Reduction in phosphoERK1/2 by inhibition of mitogen-activated protein kinase kinase (MEK) reduces neurite outgrowth of cerebellar neurons. Here, we examine the effects of ethanol on L1 activation of ERK1/2, and whether this activation occurs via activation of fibroblast growth factor receptor 1 (FGFR1). Ethanol at 25 mm markedly inhibited ERK1/2 activation by both clustering L1 with cross-linked monoclonal antibodies, or by L1-Fc chimeric proteins. Clustering L1 with subsequent ERK1/2 activation did not result in tyrosine phosphorylation of the FGFR1. In addition, inhibition of FGFR1 tyrosine kinase blocked basic fibroblast growth factor (bFGF) activation of ERK1/2, but did not affect activation of ERK1/2 by clustered L1. We conclude 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.

Indexed as

AnimalsAnimals, NewbornBlotting, WesternCells, CulturedCentral Nervous System DepressantsCerebellumDose-Response Relationship, DrugDrug InteractionsEnzyme ActivationEnzyme InhibitorsEthanolExtracellular Signal-Regulated MAP KinasesHumansImmunohistochemistryImmunoprecipitationIndoles3-(4-dimethylamino-benzylidenyl)-2-indolinoneCentral Nervous System DepressantsEnzyme InhibitorsEthanolExtracellular Signal-Regulated MAP KinasesFgfr1 protein, ratIndolesNeural Cell Adhesion Molecule L1Receptor, Fibroblast Growth Factor, Type 1

Identifiers

PMID16478533
PMCPMC4362514
OpenAlexW1611867296

What OpenQuestion holds

Textmetadata
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.