Evidence map›Paper›PMID 27392094›Full record

ArticlePloS one2016

Reverse Signaling by Semaphorin-6A Regulates Cellular Aggregation and Neuronal Morphology.

Francesc Perez-Branguli, Yvrick Zagar, Daniel K Shanley, Isabella A Graef, Alain Chédotal, Kevin J Mitchell

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 12% 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, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Semaphorins and Their Role in Neuropathic Pain.Life (Basel, Switzerland) · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Semaphorin 6A phase separation sustains a histone lactylation-dependent lactate buildup in pathological angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Variability in Neural Circuit Formation.Cold Spring Harbor perspectives in biology · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  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

6 authors at 3 institutions in 3 countries.

Francesc Perez-BranguliSmurfit Institute of Genetics and Institute of Neuroscience, Trinity College Dublin, Dublin 2, Ireland.
Yvrick ZagarSorbonne Universités, UPMC Univ Paris 06, INSERM UMR_S968, CNRS_UMR7210, Institut de la Vision, Paris, France.
Daniel K ShanleySmurfit Institute of Genetics and Institute of Neuroscience, Trinity College Dublin, Dublin 2, Ireland.
Isabella A GraefDepartment of Pathology, Stanford University Medical School, Stanford, California, United States of America.
Alain ChédotalSorbonne Universités, UPMC Univ Paris 06, INSERM UMR_S968, CNRS_UMR7210, Institut de la Vision, Paris, France.
Kevin J MitchellSmurfit Institute of Genetics and Institute of Neuroscience, Trinity College Dublin, Dublin 2, Ireland.
Trinity College Dublin · IEInserm · FRStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transmembrane semaphorin, Sema6A, has important roles in axon guidance, cell migration and neuronal connectivity in multiple regions of the nervous system, mediated by context-dependent interactions with plexin receptors, PlxnA2 and PlxnA4. Here, we demonstrate that Sema6A can also signal cell-autonomously, in two modes, constitutively, or in response to higher-order clustering mediated by either PlxnA2-binding or chemically induced multimerisation. Sema6A activation stimulates recruitment of Abl to the cytoplasmic domain of Sema6A and phos¡phorylation of this cytoplasmic tyrosine kinase, as well as phosphorylation of additional cytoskeletal regulators. Sema6A reverse signaling affects the surface area and cellular complexity of non-neuronal cells and aggregation and neurite formation of primary neurons in vitro. Sema6A also interacts with PlxnA2 in cis, which reduces binding by PlxnA2 of Sema6A in trans but not vice versa. These experiments reveal the complex nature of Sema6A biochemical functions and the molecular logic of the context-dependent interactions between Sema6A and PlxnA2.

Indexed as

AnimalsCell MovementCytoplasmCytoskeletal ProteinsMiceMicrofilament ProteinsNerve Tissue ProteinsNIH 3T3 CellsPhosphorylationProtein BindingProtein MultimerizationProtein-Tyrosine KinasesProto-Oncogene Proteins c-ablReceptors, Cell SurfaceSemaphorinsSignal TransductionCytoskeletal ProteinsEnah protein, mouseMicrofilament ProteinsNerve Tissue ProteinsPlxna2 protein, mouseProtein-Tyrosine KinasesProto-Oncogene Proteins c-ablReceptors, Cell SurfaceSemaphorins

Identifiers

PMID27392094
PMCPMC4938514
OpenAlexW2462850400

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.