Evidence map›Paper›PMID 26802239›Full record

ArticleThe Journal of investigative dermatology2016

Membrane-Tethered Intracellular Domain of Amphiregulin Promotes Keratinocyte Proliferation.

Stefan W Stoll, Philip E Stuart, Sylviane Lambert, Alberto Gandarillas, Laure Rittié, Andrew Johnston, James T Elder

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Trial
  2. Article
  3. Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Mechanisms forFrontiers in allergy · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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 2 institutions in 2 countries.

Stefan W StollDepartment of Dermatology, University of Michigan, Ann Arbor, Michigan, USA. Electronic address: sstoll@umich.edu.
Philip E StuartDepartment of Dermatology, University of Michigan, Ann Arbor, Michigan, USA.
Sylviane LambertDepartment of Dermatology, University of Michigan, Ann Arbor, Michigan, USA.
Alberto GandarillasCell Cycle, Stem Cells and Cancer Lab, Instituto de Investigación Marques de Valdecilla (IDIVAL), Santander, Spain.
Laure RittiéDepartment of Dermatology, University of Michigan, Ann Arbor, Michigan, USA.
Andrew JohnstonDepartment of Dermatology, University of Michigan, Ann Arbor, Michigan, USA.
James T ElderDepartment of Dermatology, University of Michigan, Ann Arbor, Michigan, USA; Ann Arbor Veterans Affairs Health System, Ann Arbor, Michigan, USA.
University of Michigan · USInstituto de Investigación Marqués de Valdecilla · ES

Funding

Amphiregulin in Psoriatic Epidermal HyperplasiaR01AR052889 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELDER, JAMES TILFORD · 2006 to 2010
$1.4M
Biologic Activities of IL-36 Cytokines in PsoriasisK01AR064765 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JOHNSTON, ANDREW · 2013 to 2017
$506k
Metalloproteinase regulation of ErbB signaling in skinK01AR050462 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI STOLL, STEFAN W · 2006 to 2010
$489k
Metalloproteinase regulation of ErbB signaling in skinR03AR049420 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI STOLL, STEFAN W · 2004 to 2006
$227k
NIAMS NIH HHS K01 AR050462NIAMS NIH HHS K01 AR064765NIAMS NIH HHS R01 AR 052889NIAMS NIH HHS R01 AR052889NIAMS NIH HHS R03 AR049420
6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR) and its ligands are essential regulators of epithelial biology, which are often amplified in cancer cells. We have previously shown that shRNA-mediated silencing of one of these ligands, amphiregulin (AREG), results in keratinocyte growth arrest that cannot be rescued by soluble extracellular EGFR ligands. To further explore the functional importance of specific AREG domains, we stably transduced keratinocytes expressing tetracycline-inducible AREG-targeted shRNA with lentiviruses expressing silencing-proof, membrane-tethered AREG cytoplasmic and extracellular domains (AREG-CTD and AREG-ECD), as well as full-length AREG precursor (proAREG). Here we show that growth arrest of AREG-silenced keratinocytes occurs in G2/M and is significantly restored by proAREG and AREG-CTD but not by AREG-ECD. Moreover, the AREG-CTD was sufficient to normalize cell cycle distribution profiles and expression of mitosis-related genes. Our findings uncover an important role of the AREG-CTD in regulating cell division, which may be relevant to tumor resistance to EGFR-directed therapies.

Indexed as

Gene Expression RegulationGene SilencingAmphiregulinAnimalsBlotting, WesternCell ProliferationCells, CulturedEGF Family of ProteinsEnzyme-Linked Immunosorbent AssayErbB ReceptorsFlow CytometryFluorescent Antibody TechniqueHumansKeratinocytesMiceMice, KnockoutAmphiregulinAreg protein, mouseEGF Family of ProteinsErbB ReceptorsRNA, MessengerRNA, Small Interfering

Identifiers

PMID26802239
PMCPMC4788462
OpenAlexW2275664399

What OpenQuestion holds

Textmetadata
LicenceTDM
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.