Evidence map›Paper›PMID 24344238›Full record

ArticleThe Journal of experimental medicine2014

Jab1 regulates Schwann cell proliferation and axonal sorting through p27.

Emanuela Porrello, Cristina Rivellini, Giorgia Dina, Daniela Triolo, Ubaldo Del Carro, Daniela Ungaro, Martina Panattoni, Maria Laura Feltri, Lawrence Wrabetz, Ruggero Pardi and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Peripheral Nerve Development and the Pathogenesis of Peripheral Neuropathy: the Sorting Point.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Associations and prognostic significance of p27Molecular and clinical oncology · 2016
    Article
  18. Article
  19. How Schwann Cells Sort Axons: New Concepts.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2016
    Review
  20. Review
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

12 authors at 2 institutions in 2 countries.

Emanuela PorrelloInstitute of Experimental Neurology (INSPE), Division of Neuroscience; 2 Department of Neurology; and 3 Division of Immunology, Transplantation, and Infectious Disease; San Raffaele Scientific Institute, 20132 Milan, Italy.
Cristina Rivellini
Giorgia Dina
Daniela Triolo
Ubaldo Del Carro
Daniela Ungaro
Martina Panattoni
Maria Laura Feltri
Lawrence Wrabetz
Ruggero Pardi
Angelo Quattrini
Stefano Carlo Previtali
Vita-Salute San Raffaele University · ITUniversity at Buffalo, State University of New York · US

Funding

Laminin Receptors and Signals in Schwann CellsR01NS045630 · NINDS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SIM, FRASER JAMES · 2003 to 2024
$5.9M
NINDS NIH HHS R01 NS045630NINDS NIH HHS R01NS NS045630Telethon GGP12024
6 · The paper itself

Abstract

Axonal sorting is a crucial event in nerve formation and requires proper Schwann cell proliferation, differentiation, and contact with axons. Any defect in axonal sorting results in dysmyelinating peripheral neuropathies. Evidence from mouse models shows that axonal sorting is regulated by laminin211- and, possibly, neuregulin 1 (Nrg1)-derived signals. However, how these signals are integrated in Schwann cells is largely unknown. We now report that the nuclear Jun activation domain-binding protein 1 (Jab1) may transduce laminin211 signals to regulate Schwann cell number and differentiation during axonal sorting. Mice with inactivation of Jab1 in Schwann cells develop a dysmyelinating neuropathy with axonal sorting defects. Loss of Jab1 increases p27 levels in Schwann cells, which causes defective cell cycle progression and aberrant differentiation. Genetic down-regulation of p27 levels in Jab1-null mice restores Schwann cell number, differentiation, and axonal sorting and rescues the dysmyelinating neuropathy. Thus, Jab1 constitutes a regulatory molecule that integrates laminin211 signals in Schwann cells to govern cell cycle, cell number, and differentiation. Finally, Jab1 may constitute a key molecule in the pathogenesis of dysmyelinating neuropathies.

Indexed as

AnimalsAxonsBlotting, WesternBody Weights and MeasuresBromodeoxyuridineCell DifferentiationCell ProliferationCOP9 Signalosome ComplexCyclin-Dependent Kinase Inhibitor p27ImmunohistochemistryIn Situ Nick-End LabelingIntracellular Signaling Peptides and ProteinsLamininMiceMice, KnockoutNeurogenesisBromodeoxyuridineCOP9 Signalosome ComplexCops5 protein, mouseCyclin-Dependent Kinase Inhibitor p27Intracellular Signaling Peptides and ProteinsLamininPeptide Hydrolases

Identifiers

PMID24344238
PMCPMC3892969
OpenAlexW2101597171

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.