Evidence map›Paper›PMID 24891618›Full record

ArticleMolecular and cellular biology2014

Overexpression of epigen during embryonic development induces reversible, epidermal growth factor receptor-dependent sebaceous gland hyperplasia.

Maik Dahlhoff, Daniela Frances, Jennifer E Kloepper, Ralf Paus, Matthias Schäfer, Catherin Niemann, Marlon R Schneider

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  15. Review
  16. miRNAs Are Required for Postinduction Stage Sweat Gland Development.The Journal of investigative dermatology · 2017
    Article
  17. Tregs: Where We Are and What Comes Next?Frontiers in immunology · 2017
    Review
  18. Genetically modified laboratory mice with sebaceous glands abnormalities.Cellular and molecular life sciences : CMLS · 2016
    Review
  19. Article
  20. 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

7 authors at 5 institutions in 3 countries.

Maik DahlhoffGene Center, LMU Munich, Munich, Germany.
Daniela FrancesCenter for Molecular Medicine Cologne, University of Cologne, Cologne, Germany.
Jennifer E KloepperDepartment of Dermatology, University of Lübeck, Lübeck, Germany.
Ralf PausDepartment of Dermatology, University of Muenster, Muenster, Germany Institute of Inflammation and Repair, University of Manchester, Manchester, United Kingdom.
Matthias SchäferInstitute of Molecular Health Sciences, ETH Zurich, Zurich, Switzerland.
Catherin NiemannCenter for Molecular Medicine Cologne, University of Cologne, Cologne, Germany Center for Biochemistry, Medical Faculty, University of Cologne, Cologne, Germany.
Marlon R SchneiderGene Center, LMU Munich, Munich, Germany marlon.schneider@lmu.de.
Ludwig-Maximilians-Universität München · DEUniversity of Cologne · DEETH Zurich · CHUniversity of Lübeck · DEUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR) system is a key regulator of epithelial development and homeostasis. Its functions in the sebaceous gland (SG), however, remain poorly characterized. In this study, using a transgenic mouse line with tissue-specific and inducible expression of the EGFR ligand epigen, we showed that increased activation of the EGFR in skin keratinocytes results in enlarged SGs and increased sebum production. The phenotype can be reverted by interrupting transgene expression and is EGFR dependent, as gland size and sebum levels return to normal values after crossing to the EGFR-impaired mouse line Wa5. Intriguingly, however, the SG enlargement appears only if EGFR activation occurs before birth. Importantly, the enlarged sebaceous glands are associated with an increased expression of the transcription factor MYC and of the transmembrane proteins LRIG1, an established negative-feedback regulator of the EGFR/ERBB tyrosine kinase receptors and a stem cell marker. Our findings identify EGFR signaling as a major pathway determining SG activity and suggest a functional relationship between the EGFR/ERBB system and MYC/LRIG1 in the commitment of stem cells toward specific progenitor cell types, with implications for our understanding of their role in tissue development, homeostasis, and disease.

Indexed as

AnimalsEpidermal Growth FactorEpidermisEpigenErbB ReceptorsHair FollicleHyperplasiaKeratinocytesMembrane GlycoproteinsMiceMice, TransgenicNerve Tissue ProteinsProto-Oncogene Proteins c-mycSebaceous GlandsSebumSignal TransductionEGFR protein, mouseEpgn protein, mouseEpidermal Growth FactorEpigenErbB ReceptorsLrig1 protein, mouseMembrane GlycoproteinsNerve Tissue ProteinsProto-Oncogene Proteins c-myc

Identifiers

PMID24891618
PMCPMC4135600
OpenAlexW2106738635

What OpenQuestion holds

Textmetadata
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.