Evidence map›Paper›PMID 26940862›Full record

ArticleThe Journal of investigative dermatology2016

The Notch Intracellular Domain Has an RBPj-Independent Role during Mouse Hair Follicular Development.

Mustafa Turkoz, R Reid Townsend, Raphael Kopan

Open access · greenAbstract readComparative Study
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
0.9field-weighted citation impact, top 24% 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, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Molecular therapy. Methods & clinical development · 2021
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. The Varied Roles of Notch in Cancer.Annual review of pathology · 2017
    Review
  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

3 authors at 2 institutions in 1 country.

Mustafa TurkozDivision of Developmental Biology, Children's Hospital Medical Center, Cincinnati, Ohio, USA; Department of Developmental Biology, Washington University School of Medicine, Saint Louis, Missouri, USA.
R Reid TownsendDepartment of Medicine, Washington University School of Medicine, Saint Louis, Missouri, USA; Department of Cell Biology and Physiology, Washington University School of Medicine, Saint Louis, Missouri, USA.
Raphael KopanDivision of Developmental Biology, Children's Hospital Medical Center, Cincinnati, Ohio, USA; Department of Developmental Biology, Washington University School of Medicine, Saint Louis, Missouri, USA. Electronic address: Raphael.Kopan@cchmc.org.
Cincinnati Children's Hospital Medical Center · USWashington University in St. Louis · US

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
Washington University Institute of Clinical and Translational SciencesUL1TR000448 · NCATS · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2012 to 2016
$41.4M
BIOCHEMICAL AND GENETIC ANALYSIS OF NOTCH SIGNALINGR01GM055479 · NIGMS · WASHINGTON UNIVERSITY · PI KOPAN, RAPHAEL, WEIRAUCH, MATTHEW TYSON · 1996 to 2021
$6.4M
NCATS NIH HHS UL1 TR000448NCI NIH HHS P30 CA091842NIGMS NIH HHS R01 GM055479
6 · The paper itself

Abstract

Ligand-dependent activation, γ-secretase-processed cleavage, and recombining binding protein Jk (RBPj)-mediated downstream transcriptional activities of Notch receptors constitute the "canonical" Notch signaling pathway, which is essential for skin organogenesis. However, in Msx2-Cre mice, keratinocyte-specific deletion of the Rbpj gene in utero produced a significantly milder phenotype than either global Notch or γ-secretase loss. Herein, we investigated the underlying mechanisms for this apparent noncanonical signal using mouse genetics. We found no evidence that ligand back-signaling contributed to skin organogenesis. The perdurance of RBPj protein did not establish an epigenetic memory of a canonical signal in the youngest epidermal stem cells, and Notch targets were not derepressed. We provide evidence that γ-secretase-dependent but RBPj-independent Notch intracellular domain activity operating in the first hair follicles is responsible for a delay in follicular destruction, which results in lower serum thymic stromal lymphopoietin levels, milder B-cell lymphoproliferative disease, and improved survival in Msx2-Cre(+/tg);Rbpj(f/f) mice. Minimal amounts of the Notch intracellular domain were sufficient for rescue, which was not mediated by transcription, suggesting that the Notch intracellular domain is acting through a novel mechanism.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsCells, CulturedEpithelial CellsHairHair FollicleHumansImmunoglobulin J Recombination Signal Sequence-Binding ProteinMaleMiceMice, TransgenicPhenotypeReal-Time Polymerase Chain ReactionReceptors, NotchRoleSignal TransductionImmunoglobulin J Recombination Signal Sequence-Binding ProteinRbpj protein, mouseReceptors, Notch

Identifiers

PMID26940862
PMCPMC5036938
OpenAlexW2292687456

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.