Evidence map›Paper›PMID 21182951›Full record

ArticleMolecular and cellular neurosciences2011

Schwannomin/merlin promotes Schwann cell elongation and influences myelin segment length.

Courtney Thaxton, Marga Bott, Barbara Walker, Nicklaus A Sparrow, Stephen Lambert, Cristina Fernandez-Valle

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular neurosciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. A neuronal function of the tumor suppressor protein merlin.Acta neuropathologica communications · 2014
    Review
  14. Article
  15. Article
  16. Article
  17. Rac1 controls Schwann cell myelination through cAMP and NF2/merlin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  18. The actin-severing protein cofilin is downstream of neuregulin signaling and is essential for Schwann cell myelination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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

6 authors at 2 institutions in 1 country.

Courtney ThaxtonDepartment of Molecular Biology and Microbiology, Burnett School of Biomedical Science, College of Medicine, University of Central Florida, Health Science Campus, 6900 Lake Nona Boulevard, Orlando, FL 32827, USA.
Marga Bott
Barbara Walker
Nicklaus A Sparrow
Stephen Lambert
Cristina Fernandez-Valle
University of Central Florida · USUniversity of Massachusetts Chan Medical School · US

Funding

Identification of Novel Drug Targets For Use in Preventing Deafness Caused by NF2R01DC010189 · NIDCD · UNIVERSITY OF CENTRAL FLORIDA · PI FERNANDEZ-VALLE, CRISTINA MARIA · 2009 to 2013
$1.4M
Mechanisms Modulating Cytoskeletal Dynamics During Schwann Cell MyelinationR01NS062825 · NINDS · UNIVERSITY OF CENTRAL FLORIDA · PI FERNANDEZ-VALLE, CRISTINA MARIA · 2009 to 2010
$722k
NIDCD NIH HHS 1R01DC010189-01NIDCD NIH HHS R01 DC010189NINDS NIH HHS R01 NS062825
6 · The paper itself

Abstract

The Neurofibromatosis type 2 tumor suppressor, schwannomin (Sch) is a plasma membrane-cytoskeleton linking protein that regulates receptor signaling and actin dynamics. We examined Sch's role in specifying morphological changes needed for Schwann cell (SC) function in vitro. Isolated Sch-GFP-expressing SCs extended bipolar processes 82% longer than those formed by GFP-expressing cells. In contrast, SCs expressing dominant negative Sch-BBA-GFP extended bipolar processes 16% shorter than controls and 64% shorter than Sch-GFP-expressing SCs. nf2 gene inactivation caused isolated mouse SCs to transition from bipolar to multipolar cells. Live imaging revealed that SCs co-expressing Sch-GFP and dominant negative RacN17 behaved similarly in dorsal root ganglion explant cultures; they quickly aligned on axons and slowly elongated bipolar processes. In contrast, SCs expressing constitutively active RacV12 underwent continuous transitions in morphology that interfered with axon alignment. When co-cultured with neurons under myelin-promoting conditions, Sch-GFP-expressing SCs elaborated longer myelin segments than GFP-expressing SCs. In contrast, Sch-BBA-GFP-expressing SCs failed to align on or myelinate axons. Together, these results demonstrate that Sch plays an essential role in inducing and/or maintaining the SC's spindle shape and suggest that the mechanism involves Sch-dependent inhibition of Rac activity. By stabilizing the bipolar morphology, Sch promotes the alignment of SCs with axons and ultimately influences myelin segment length.

Indexed as

AcetazolamideAnimalsCells, CulturedCoculture TechniquesGanglia, SpinalMiceMyelin SheathNerve Fibers, MyelinatedNeurofibromatosis 2Neurofibromin 2rac GTP-Binding ProteinsRatsRats, Sprague-DawleyRats, WistarRecombinant Fusion ProteinsSchwann CellsAcetazolamideNeurofibromin 2rac GTP-Binding ProteinsRecombinant Fusion Proteins

Identifiers

PMID21182951
PMCPMC3129596
OpenAlexW2033778954

What OpenQuestion holds

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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.