Evidence map›Paper›PMID 24638168›Full record

ArticleThe Journal of experimental medicine2014

Dynamin 2-dependent endocytosis is required for sustained S1PR1 signaling.

Tim Willinger, Shawn M Ferguson, João P Pereira, Pietro De Camilli, Richard A Flavell

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 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Transmembrane protein CD69 acts as an S1PR1 agonist.bioRxiv : the preprint server for biology · 2023
    Article
  8. Article
  9. Tetraspanin CD82 regulates S1PRStem cell reports · 2021
    Article
  10. Article
  11. Article
  12. C-Cbl regulates c-MPL receptor trafficking and its internalization.Journal of cellular and molecular medicine · 2020
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. IL-10 Paradoxically Promotes Autoimmune Neuropathy through S1PR1-Dependent CD4Journal of immunology (Baltimore, Md. : 1950) · 2018
    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

5 authors at 3 institutions in 2 countries.

Tim WillingerDepartment of Immunobiology, 2 Department of Cell Biology, 3 Program in Cellular Neuroscience, Neurodegeneration, and Repair, and 4 Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520.
Shawn M Ferguson
João P Pereira
Pietro De Camilli
Richard A Flavell
Institute of Cell Biology · UAHoward Hughes Medical Institute · USYale University · US

Funding

Molecular Mechanisms in Synaptic Vesicle RecyclingR37NS036251 · NINDS · YALE UNIVERSITY · PI DE CAMILLI, PIETRO · 2010 to 2016
$2.7M
NINDS NIH HHS R37 NS036251NINDS NIH HHS R37NS036251
6 · The paper itself

Abstract

Sphingosine-1-phosphate (S1P) receptor 1 (S1PR1) is critical for lymphocyte egress from lymphoid organs. Lymphocytes encounter low S1P concentrations near exit sites before transmigration, yet S1PR1 signaling is rapidly terminated after exposure to S1P. How lymphocytes maintain S1PR1 signaling in a low S1P environment near egress sites is unknown. Here we identify dynamin 2, an essential component of endocytosis, as a novel regulator of T cell egress. Mice with T cell-specific dynamin 2 deficiency had profound lymphopenia and impaired egress from lymphoid organs. Dynamin 2 deficiency caused impaired egress through regulation of S1PR1 signaling, and transgenic S1PR1 overexpression rescued egress in dynamin 2 knockout mice. In low S1P concentrations, dynamin 2 was essential for S1PR1 internalization, which enabled continuous S1PR1 signaling and promoted egress from both thymus and lymph nodes. In contrast, dynamin 2-deficient cells were only capable of a pulse of S1PR1 signaling, which was insufficient for egress. Our results suggest a possible mechanism by which T lymphocytes positioned at exit portals sense low S1P concentrations, promoting their egress into circulatory fluids.

Indexed as

EndocytosisSignal TransductionAnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteCD69 AntigensChemotaxisDynamin IIGTP-Binding Protein alpha Subunits, Gi-GoLectins, C-TypeLigandsLymph NodesLymphopeniaLysophospholipidsMiceMice, KnockoutAntigens, CDAntigens, Differentiation, T-LymphocyteCD69 AntigensDynamin IIGnai1 protein, mouseGTP-Binding Protein alpha Subunits, Gi-GoLectins, C-TypeLigandsLysophospholipidsReceptors, ChemokineReceptors, G-Protein-CoupledReceptors, LysosphingolipidSphingosinesphingosine 1-phosphate

Identifiers

PMID24638168
PMCPMC3978280
OpenAlexW2119490807

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.