Evidence map›Paper›PMID 24358210›Full record

ArticlePloS one2013

Moesin controls clathrin-mediated S1PR1 internalization in T cells.

Akira Nomachi, Masanori Yoshinaga, Jaron Liu, Pakorn Kanchanawong, Kiyoshi Tohyama, Dean Thumkeo, Takeshi Watanabe, Shuh Narumiya, Takako Hirata

Abstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Post-translational modifications of S1PR1 and endothelial barrier regulation.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020
    Review
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  8. Review
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  10. Article
  11. Article
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  15. 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

9 authors.

Akira NomachiCenter for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Masanori YoshinagaDepartment of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Jaron LiuMechanobiology Institute, Singapore, Singapore.
Pakorn KanchanawongMechanobiology Institute, Singapore, Singapore ; Department of Bioengineering, National University of Singapore, Singapore, Singapore.
Kiyoshi TohyamaDepartment of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Dean ThumkeoDepartment of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Takeshi WatanabeCenter for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Shuh NarumiyaCenter for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Japan ; Department of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Takako HirataDepartment of Fundamental Biosciences, Shiga University of Medical Science, Otsu, Shiga, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The lipid mediator sphingosine 1-phosphate (S1P) regulates a wide range of cellular activities, including vascular maturation, angiogenesis, and immune-cell trafficking. Among the five known receptors for S1P (S1PR1-S1PR5), S1PR1 is a critical regulator of lymphocyte trafficking: its signaling is required for lymphocyte egress from lymphoid organs, while its down-modulation by agonist-induced internalization is a prerequisite for lymphocyte entry into lymphoid organs from the bloodstream. Despite the importance of S1PR1 down-regulation in determining lymphocyte behavior, the molecular mechanism of its internalization in lymphocytes has not been defined. Here we show that agonist-induced S1PR1 internalization in T cells occurs via clathrin-mediated endocytosis and is regulated by moesin, an ezrin-radixin-moesin (ERM) family member. In S1P-stimulated T cells, S1PR1 relocalized within clathrin-coated vesicles (CCVs) and early endosomes, and S1PR1 internalization was blocked when clathrin was pharmacologically inhibited. Stimulating moesin-deficient T cells with S1P failed to induce S1PR1 internalization and CCV formation. Furthermore, treating moesin-deficient mice with FTY720, an S1P receptor agonist known to internalize S1PR1, caused delayed lymphopenia, and lymphocytes isolated from FTY720-treated moesin-deficient mice still responded to S1P ex vivo in chemotaxis assays. These results reveal a novel role for moesin in regulating clathrin-dependent S1PR1 internalization through CCV formation.

Indexed as

AnimalsCD4-Positive T-LymphocytesCells, CulturedChemotaxis, LeukocyteClathrin-Coated VesiclesEndocytosisHEK293 CellsHumansMaleMiceMice, Inbred C57BLMice, KnockoutMicrofilament ProteinsReceptors, LysosphingolipidSphingosine-1-Phosphate ReceptorsMicrofilament ProteinsmoesinReceptors, LysosphingolipidS1pr1 protein, mouseSphingosine-1-Phosphate Receptors

Identifiers

PMID24358210
PMCPMC3865155

What OpenQuestion holds

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LicenceCC BY
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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.