Evidence map›Paper›PMID 20576928›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2011

L1 and CHL1 Cooperate in Thalamocortical Axon Targeting.

Galina P Demyanenko, Priscila F Siesser, Amanda G Wright, Leann H Brennaman, Udo Bartsch, Melitta Schachner, Patricia F Maness

Open access · bronzeAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Axonal Growth of Midbrain Dopamine Neurons is Modulated by the Cell Adhesion Molecule ALCAM ThroughThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  7. Close Homolog of L1 Regulates Dendritic Spine Density in the Mouse Cerebral Cortex Through Semaphorin 3B.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. MicroRNA-Mediated Regulation ofFrontiers in molecular neuroscience · 2017
    Article
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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 3 institutions in 3 countries.

Galina P DemyanenkoDepartment of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
Priscila F Siesser
Amanda G Wright
Leann H Brennaman
Udo Bartsch
Melitta Schachner
Patricia F Maness
University of North Carolina at Chapel Hill · USRutgers, The State University of New Jersey · USUniversität Hamburg · DE

Funding

Recognition Molecules in Cortical DevelopmentR01NS049109 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MANESS, PATRICIA F · 2005 to 2008
$1.1M
NIMH NIH HHS MH064056NINDS NIH HHS NS049109
6 · The paper itself

Abstract

Neural cell adhesion molecule close homolog of L1 (CHL1) is a regulator of topographic targeting of thalamic axons to the somatosensory cortex (S1) but little is known about its cooperation with other L1 class molecules. To investigate this, CHL1(-/-)/L1(-/y) double mutant mice were generated and analyzed for thalamocortical axon topography. Double mutants exhibited a striking posterior shift of axons from motor thalamic nuclei to the visual cortex (V1), which was not observed in single mutants. In wild-type (WT) embryos, L1 and CHL1 were coexpressed in the dorsal thalamus (DT) and on fibers along the thalamocortical projection in the ventral telencephalon and cortex. L1 and CHL1 colocalized on growth cones and neurites of cortical and thalamic neurons in culture. Growth cone collapse assays with WT and mutant neurons demonstrated a requirement for L1 and CHL1 in repellent responses to EphrinA5, a guidance factor for thalamic axons. L1 coimmunoprecipitated with the principal EphrinA5 receptors expressed in the DT (EphA3, EphA4, and EphA7), whereas CHL1 associated selectively with EphA7. These results implicate a novel mechanism in which L1 and CHL1 interact with individual EphA receptors and cooperate to guide subpopulations of thalamic axons to distinct neocortical areas essential for thalamocortical connectivity.

Indexed as

Amino AcidsAnimalsAxonsCell Adhesion MoleculesCells, CulturedCerebral CortexEmbryo, MammalianEphrin-A5Gene Expression RegulationGrowth ConesHumansImmunoprecipitationLuminescent ProteinsMiceMice, Inbred C57BLMice, TransgenicAmino AcidsCell Adhesion MoleculesChl1 protein, mousedolaisoleucineEphrin-A5Luminescent ProteinsNeural Cell Adhesion Molecule L1Receptors, Eph Family

Identifiers

PMID20576928
PMCPMC3020587
OpenAlexW2107007724

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.