Evidence map›Paper›PMID 11956225›Full record

ArticleThe Journal of cell biology2002

An inactive pool of GSK-3 at the leading edge of growth cones is implicated in Semaphorin 3A signaling.

Britta J Eickholt, Frank S Walsh, Patrick Doherty

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

94 citing papers in PubMed, 242 citations in OpenAlex.

  1. Article
  2. Article
  3. Unleashing Intrinsic Growth Pathways in Regenerating Peripheral Neurons.International journal of molecular sciences · 2022
    Review
  4. The Nogo-66 Receptors NgR1 and NgR3 Are Required for Commissural Axon Pathfinding.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  5. Article
  6. Neurobiological Opportunities in Diabetic Polyneuropathy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Review
  7. Article
  8. Review
  9. Review
  10. Semaphorins in Adult Nervous System Plasticity and Disease.Frontiers in synaptic neuroscience · 2021
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. PTEN in Autism and Neurodevelopmental Disorders.Cold Spring Harbor perspectives in medicine · 2019
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

34 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Britta J EickholtMolecular Neurobiology Group, Medical Research Council Centre for Developmental Biology, King's College London, London SE1 1UL, United Kingdom. Britta.J.Eickholt@kcl.ac.uk
Frank S Walsh
Patrick Doherty
Medical Research Council · GBGlaxoSmithKline (United Kingdom) · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycogen synthase kinase (GSK)-3 is a serine/threonine kinase that has been implicated in several aspects in embryonic development and several growth factor signaling cascades. We now report that an inactive phosphorylated pool of the enzyme colocalizes with F-actin in both neuronal and nonneuronal cells. Semaphorin 3A (Sema 3A), a molecule that inhibits axonal growth, activates GSK-3 at the leading edge of neuronal growth cones and in Sema 3A-responsive human breast cancer cells, suggesting that GSK-3 activity might play a role in coupling Sema 3A signaling to changes in cell motility. We show that three different GSK-3 antagonists (LiCl, SB-216763, and SB-415286) can inhibit the growth cone collapse response induced by Sema 3A. These studies reveal a novel compartmentalization of inactive GSK-3 in cells and demonstrate for the first time a requirement for GSK-3 activity in the Sema 3A signal transduction pathway.

Indexed as

Signal TransductionActinsAnimalsBlotting, WesternCalcium-Calmodulin-Dependent Protein KinasesCells, CulturedCell SizeChick EmbryoCOS CellsEnzyme ActivationGanglia, SpinalGlycogen Synthase Kinase 3Glycogen Synthase KinasesGlycoproteinsGrowth ConesHumansActinsCalcium-Calmodulin-Dependent Protein KinasesGlycogen Synthase Kinase 3Glycogen Synthase KinasesGlycoproteinsPhosphoinositide-3 Kinase InhibitorsSemaphorin-3A

Identifiers

PMID11956225
PMCPMC2199247
OpenAlexW2002412835

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.