Evidence map›Paper›PMID 16571745›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Temporal control of Rac in Schwann cell-axon interaction is disrupted in NF2-mutant schwannoma cells.

Yoko Nakai, Yi Zheng, Mia MacCollin, Nancy Ratner

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 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
6.0field-weighted citation impact, top 4% 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, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Schwannomas and their pathogenesis.Brain pathology (Zurich, Switzerland) · 2014
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Rac1 controls Schwann cell myelination through cAMP and NF2/merlin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  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

4 authors at 3 institutions in 1 country.

Yoko NakaiDivision of Experimental Hematology, Cincinnati Children's Hospital Research Foundation, Department of Pediatrics, University of Cincinnati, Cincinnati, Ohio 45229, USA.
Yi Zheng
Mia MacCollin
Nancy Ratner
Cincinnati Children's Hospital Medical Center · USMassachusetts General Hospital · USUniversity of Cincinnati · US

Funding

Schwann Cells in Neurofibromatosis Type 2 (NF2)R01CA118032 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI RATNER, NANCY · 2007 to 2011
$1.4M
NCI NIH HHS CA75824NCI NIH HHS R01 CA118032
6 · The paper itself

Abstract

Schwann cell-axon interaction is the hallmark feature of peripheral nerves, yet the intracellular signals underlying this interaction are unknown. Schwann cells extend processes and migrate on developing axons before differentiation, requiring coordinated regulation of the Schwann cell cytoskeleton. Small GTPases of the Rho family, including Rho, Rac, and cell division cycle 42, regulate the actin cytoskeleton. The neurofibromatosis type 2 (NF2) gene is commonly mutated in schwannomas, Schwann cell tumors that contain cells lacking axon interaction. NF2 is involved in suppression of Rac signaling, and cultured schwannoma cells contain elevated, GTP-bound, active Rac. Despite these previous studies, a causal relationship between Rac activation and the abnormal cellular morphology of schwannoma is unknown. We used fluorescence resonance energy transfer to follow Rac activity in normal human Schwann cells and schwannoma cells during interaction with neurons. Normal Schwann cells elongated processes along neurites under low Rac activity. Schwannoma cells showed high Rac activity at distal regions of the cells and failed to align processes with neurites. Application of a Rac-specific inhibitor, the chemical compound NSC23766, to schwannoma cells restored neuronal interaction. The data support the significance of regulated Rac signaling in mediating Schwann cell-axon interaction and suggest that controlling Rac activity as a possible therapy for schwannomas.

Indexed as

Cell CommunicationAxonsCells, CulturedHumansMetabolic Clearance RateNeurofibromin 2rac GTP-Binding ProteinsSchwann CellsTime FactorsNeurofibromin 2rac GTP-Binding Proteins

Identifiers

PMID16571745
PMCPMC6673872
OpenAlexW2100119912

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.