Evidence map›Paper›PMID 27597758›Full record

ArticleThe Journal of cell biology2016

Tiam-Rac signaling mediates trans-endocytosis of ephrin receptor EphB2 and is important for cell repulsion.

Thomas N Gaitanos, Jorg Koerner, Ruediger Klein

Erratum issuedOpen access · bronzeAbstract readVideo-Audio Media
In one paragraph

Article in The Journal of cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
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  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. The Roles of EphB2 in Cancer.Frontiers in cell and developmental biology · 2022
    Review
  12. Article
  13. Review
  14. Article
  15. Modular and Distinct Plexin-A4/FARP2/Rac1 Signaling Controls Dendrite Morphogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Journal of cell science · 2019
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Thomas N GaitanosDepartment of Molecules-Signaling-Development, Max Planck Institute of Neurobiology, 82152 Munich-Martinsried, Germany klein@neuro.mpg.de tgaitanos@neuro.mpg.de.ORCID http://orcid.org/0000-0002-2693-9943
Jorg KoernerDepartment of Molecules-Signaling-Development, Max Planck Institute of Neurobiology, 82152 Munich-Martinsried, Germany.ORCID http://orcid.org/0000-0003-0597-312X
Ruediger KleinDepartment of Molecules-Signaling-Development, Max Planck Institute of Neurobiology, 82152 Munich-Martinsried, Germany klein@neuro.mpg.de tgaitanos@neuro.mpg.de.ORCID http://orcid.org/0000-0002-3109-0163
Max Planck Institute of Neurobiology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ephrin receptors interact with membrane-bound ephrin ligands to regulate contact-mediated attraction or repulsion between opposing cells, thereby influencing tissue morphogenesis. Cell repulsion requires bidirectional trans-endocytosis of clustered Eph-ephrin complexes at cell interfaces, but the mechanisms underlying this process are poorly understood. Here, we identified an actin-regulating pathway allowing ephrinB(+) cells to trans-endocytose EphB receptors from opposing cells. Live imaging revealed Rac-dependent F-actin enrichment at sites of EphB2 internalization, but not during vesicle trafficking. Systematic depletion of Rho family GTPases and their regulatory proteins identified the Rac subfamily and the Rac-specific guanine nucleotide exchange factor Tiam2 as key components of EphB2 trans-endocytosis, a pathway previously implicated in Eph forward signaling, in which ephrins act as in trans ligands of Eph receptors. However, unlike in Eph signaling, this pathway is not required for uptake of soluble ligands in ephrinB(+) cells. We also show that this pathway is required for EphB2-stimulated contact repulsion. These results support the existence of a conserved pathway for EphB trans-endocytosis that removes the physical tether between cells, thereby enabling cell repulsion.

Indexed as

Cell CommunicationCell MovementEndocytosisActin CytoskeletonAnimalscdc42 GTP-Binding ProteinCoculture TechniquesGuanine Nucleotide Exchange FactorsHEK293 CellsHeLa CellsHumansMiceMicroscopy, FluorescenceNeuroblastomaNeuronsProtein Domainscdc42 GTP-Binding ProteinEPHB2 protein, humanGuanine Nucleotide Exchange Factorsrac GTP-Binding ProteinsReceptor, EphB2Recombinant Fusion ProteinsrhoA GTP-Binding ProteinRHOA protein, humanTIAM2 protein, human

Identifiers

PMID27597758
PMCPMC5021091
OpenAlexW2509825400

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.