Evidence map›Paper›PMID 10460245›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Evidence of an agrin receptor in cortical neurons.

L G Hilgenberg, C L Hoover, M A Smith

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-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

14 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Synapse loss in cortex of agrin-deficient mice after genetic rescue of perinatal death.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Agrin differentially regulates the rates of axonal and dendritic elongation in cultured hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    Article
  13. Agrin controls synaptic differentiation in hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000
    Article
  14. 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

3 authors at 1 institution in 1 country.

L G HilgenbergDepartment of Anatomy and Neurobiology, University of California at Irvine, Irvine, California 92697, USA.
C L Hoover
M A Smith
University of California, Irvine · US

Funding

AGRIN GENE EXPRESSIONR01NS033213 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI SMITH, MARTIN A · 1994 to 2009
$2.6M
NINDS NIH HHS NS33213NINDS NIH HHS R01 NS033213
6 · The paper itself

Abstract

Agrin plays a key role in directing the differentiation of the vertebrate neuromuscular junction. Understanding agrin function at the neuromuscular junction has come via molecular genetic analyses of agrin as well as identification of its receptor and associated signal transduction pathways. Agrin is also expressed by many populations of neurons in brain, but its role remains unknown. Here we show, in cultured cortical neurons, that agrin induces expression of the immediate early gene c-fos in a concentration-dependent and saturable manner, as expected for a signal transduction pathway activated by a cell surface receptor. Agrin is active in cortical neurons at picomolar concentrations, is Ca(2+) dependent, and is inhibited by heparin and staurosporine. Despite marked differences in acetylcholine receptor (AChR)-clustering activity, all alternatively spliced forms of agrin are equally potent inducers of c-fos in cortical neurons. A similar, isoform-independent response to agrin was also observed in cultures prepared from the hippocampus and cerebellum. Only agrin with high AChR-clustering activity was effective in cultured muscle, whereas non-neuronal cells were agrin insensitive. Although consistent with a receptor tyrosine kinase model similar to the muscle-specific kinase-myotube-associated specificity component complex in muscle, our data suggest that CNS neurons express a unique agrin receptor. Evidence that neuronal signal transduction is mediated via an increase in intracellular Ca(2+) means that agrin is well situated to influence important Ca(2+)-dependent functions in brain, including neuronal growth, differentiation, and adaptive changes in gene expression associated with synaptic remodeling.

Indexed as

AgrinAlternative SplicingAnimalsAnimals, NewbornCalciumCells, CulturedCerebral CortexChelating AgentsChick EmbryoCOS CellsCulture Media, ConditionedEgtazic AcidEnzyme ActivationGene Expression RegulationGenes, fosHeparin1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl esterAgrinagrin receptorCalciumChelating AgentsCulture Media, ConditionedEgtazic AcidHeparinProtein IsoformsProtein KinasesProto-Oncogene Proteins c-fosReceptors, CholinergicReceptors, Growth FactorStaurosporine

Identifiers

PMID10460245
PMCPMC6782495
OpenAlexW2171035480

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.