Evidence map›Paper›PMID 22783168›Full record

ArticleFrontiers in cellular neuroscience2012

Receptor complexes for each of the Class 3 Semaphorins.

Anil Sharma, Joost Verhaagen, Alan R Harvey

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

60 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Semaphorins and Their Role in Neuropathic Pain.Life (Basel, Switzerland) · 2026
    Review
  3. Article
  4. Semaphorin 3A and 3F Promote Lumen Expansion in TIE2-Mutated Venous Malformation.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Plexin B3 guides axons to cross the midlineFrontiers in cellular neuroscience · 2024
    Article
  9. New Promising Routes in Peptic Ulcers: Toll-like Receptors and Semaphorins.Endocrine, metabolic & immune disorders drug targets · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. A Novel Loss-of-FunctionInternational journal of molecular sciences · 2022
    Article
  16. Article
  17. Article
  18. Unraveling Axon Guidance during Axotomy and Regeneration.International journal of molecular sciences · 2021
    Review
  19. Article
  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

3 authors at 2 institutions in 2 countries.

Anil SharmaSchool of Anatomy, Physiology and Human Biology, The University of Western Australia, Crawley WA, Australia.
Joost Verhaagen
Alan R Harvey
University of Western Australia · AUNetherlands Institute for Neuroscience · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Class 3 Semaphorins (Sema3s) are a sub-family of proteins whose known biological roles are varied and growing. The mechanism of action of the Sema3s requires binding to transmembrane receptors that comprise heteromeric complexes of Neuropilins, Plexins and cell adhesion molecules (CAMs). However, knowledge of the receptor components of the Sema3s remains incomplete, and there may be receptor components which are as yet undiscovered. The receptor complexes of the Sema3s share receptor components with each other, and it is the specific combination of these components within a heteromeric complex that is thought to give rise to selective binding and signalling for individual Sema3s. This crosstalk makes it experimentally difficult to define a single holoreceptor for each Sema3. Furthermore, the receptor composition for a given Sema3 may differ between cell types, and change as a function of developmental state or pathological situation. Nevertheless, there are at least some known differences in the constitutive structure of the receptors for the Sema3s. For example in neural cells, Sema3a and Sema3f signal through different Neuropilins (Nrp1 and Nrp2 respectively) and L1cam only appears important for Sema3a signaling, while Nrcam forms a complex with Nrp2. Further complexity arises from crosstalk of other families of ligands (e.g., VEGF) with Sema3 receptor components. Thus the Sema3s, which have been shown as antagonists for each other, can also act as antagonists for other families of molecules. This review compiles experimental evidence describing the receptor components for the Sema3s, detailing the current state of knowledge of which components are important for signaling of each Sema3 before going on to consider possible future directions for the field.

Indexed as

adhesion moleculesaxon guidanceaxon repulsionNeuropilinsPlexinsRoboSemaphorins

Identifiers

PMID22783168
PMCPMC3389612
OpenAlexW2042155225

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.