Evidence map›Paper›PMID 26401001›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

The PDK1-Rsk Signaling Pathway Controls Langerhans Cell Proliferation and Patterning.

Rossana Zaru, Stephen P Matthews, Alexander J Edgar, Alan R Prescott, Diego Gomez-Nicola, André Hanauer, Colin Watts

Open access · hybridAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Therapeutic targeting of p90 ribosomal S6 kinase.Frontiers in cell and developmental biology · 2023
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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

7 authors at 3 institutions in 3 countries.

Rossana ZaruDivision of Cell Signaling and Immunology, College of Life Science, University of Dundee, Dundee DD1 5EH, United Kingdom;
Stephen P MatthewsDivision of Cell Signaling and Immunology, College of Life Science, University of Dundee, Dundee DD1 5EH, United Kingdom;
Alexander J EdgarDivision of Cell Signaling and Immunology, College of Life Science, University of Dundee, Dundee DD1 5EH, United Kingdom;
Alan R PrescottDivision of Cell Signaling and Immunology, College of Life Science, University of Dundee, Dundee DD1 5EH, United Kingdom;
Diego Gomez-NicolaCentre for Biological Sciences, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, United Kingdom; and.
André HanauerInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique Unite Mixté de Recherche 7104, INSERM U 964, University of Strasbourg, 67404 Illkirch, France.
Colin WattsDivision of Cell Signaling and Immunology, College of Life Science, University of Dundee, Dundee DD1 5EH, United Kingdom; c.watts@dundee.ac.uk.ORCID http://orcid.org/0000-0001-6183-2087
University of Dundee · GBInserm · FRSouthampton General Hospital · GB

Funding

Medical Research Council G0701272Medical Research Council MR/K022687/1Wellcome Trust 093489Wellcome Trust 093489/Z/10/ZWellcome Trust 097945
6 · The paper itself

Abstract

Langerhans cells (LC), the dendritic cells of the epidermis, are distributed in a distinctive regularly spaced array. In the mouse, the LC array is established in the first few days of life from proliferating local precursors, but the regulating signaling pathways are not fully understood. We found that mice lacking the kinase phosphoinositide-dependent kinase 1 selectively lack LC. Deletion of the phosphoinositide-dependent kinase 1 target kinases, ribosomal S6 kinase 1 (Rsk1) and Rsk2, produced a striking perturbation in the LC network: LC density was reduced 2-fold, but LC size was increased by the same magnitude. Reduced LC numbers in Rsk1/2(-/-) mice was not due to accelerated emigration from the skin but rather to reduced proliferation at least in adults. Rsk1/2 were required for normal LC patterning in neonates, but not when LC were ablated in adults and replaced by bone marrow-derived cells. Increased LC size was an intrinsic response to reduced LC numbers, reversible on LC emigration, and could be observed in wild type epidermis where LC size also correlated inversely with LC density. Our results identify a key signaling pathway needed to establish a normal LC network and suggest that LC might maintain epidermal surveillance by increasing their "footprint" when their numbers are limited.

Indexed as

Cell ProliferationSignal Transduction3-Phosphoinositide-Dependent Protein KinasesAnimalsAnimals, NewbornCell CountCell MovementCells, CulturedCell SizeEpidermal CellsEpidermisFlow CytometryLangerhans CellsMice, Inbred C57BLMice, KnockoutMicroscopy, Confocal3-Phosphoinositide-Dependent Protein Kinasesribosomal protein S6 kinase, 90kDa, polypeptide 3Ribosomal Protein S6 Kinases, 90-kDaRps6ka1 protein, mouse

Identifiers

PMID26401001
PMCPMC4640173
OpenAlexW2203711791

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.