Evidence map›Paper›PMID 17611229›Full record

ArticleDevelopment (Cambridge, England)2007

Bi-compartmental communication contributes to the opposite proliferative behavior of Notch1-deficient hair follicle and epidermal keratinocytes.

Jonghyeob Lee, Jacob M Basak, Shadmehr Demehri, Raphael Kopan

Open access · greenAbstract readComparative Study
In one paragraph

Article in Development (Cambridge, England), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
9.6field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Characterization and angiogenic potential of CD146Stem cell research & therapy · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Cancer Stem Cells,Cells · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Cutaneous Notch signaling in health and disease.Cold Spring Harbor perspectives in medicine · 2013
    Review
  18. Article
  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

4 authors at 1 institution in 1 country.

Jonghyeob LeeDepartment of Molecular Biology and Pharmacology, Washington University School of Medicine, Box 8103, 660 South Euclid Avenue, Saint Louis, MO 63110, USA.
Jacob M Basak
Shadmehr Demehri
Raphael Kopan
Washington University in St. Louis · US

Funding

BIOCHEMICAL AND GENETIC ANALYSIS OF NOTCH SIGNALINGR01GM055479 · NIGMS · WASHINGTON UNIVERSITY · PI KOPAN, RAPHAEL, WEIRAUCH, MATTHEW TYSON · 1996 to 2021
$6.4M
Mapping Notch 1 Activation in MiceR01HD044056 · NICHD · WASHINGTON UNIVERSITY · PI KOPAN, RAPHAEL · 2003 to 2007
$1.7M
NICHD NIH HHS R01 HD044056NIGMS NIH HHS GM55479-10NIGMS NIH HHS R01 GM055479
6 · The paper itself

Abstract

Notch1-deficient epidermal keratinocytes become progressively hyperplastic and eventually produce tumors. By contrast, Notch1-deficient hair matrix keratinocytes have lower mitotic rates, resulting in smaller follicles with fewer cells. In addition, the ratio of melanocytes to keratinocytes is greatly reduced in hair follicles. Investigation into the underlying mechanism for these phenotypes revealed significant changes in the Kit, Tgfbeta and insulin-like growth factor (IGF) signaling pathways, which have not been previously shown to be downstream of Notch signaling. The level of Kitl (Scf) mRNA produced by Notch1-deficient follicular keratinocytes was reduced when compared with wild type, resulting in a decline in melanocyte population. Tgfbeta ligands were elevated in Notch1-deficient keratinocytes, which correlated with elevated expression of several targets, including the diffusible IGF antagonist Igfbp3 in the dermal papilla. Diffusible stromal targets remained elevated in the absence of epithelial Tgfbeta receptors, consistent with paracrine Tgfbeta signaling. Overexpression of Igf1 in the keratinocyte reversed the phenotype, as expected if Notch1 loss altered the IGF/insulin-like growth factor binding protein (IGFBP) balance. Conversely, epidermal keratinocytes contained less stromal Igfbp4 and might thus be primed to experience an increase in IGF signaling as animals age. These results suggest that Notch1 participates in a bi-compartmental signaling network that controls homeostasis, follicular proliferation rates and melanocyte population within the skin.

Indexed as

Cell ProliferationEpidermal CellsAnimalsApoptosis Regulatory ProteinsCell CommunicationCell CompartmentationCell CountEpidermisFemaleHair FollicleKeratinocytesMaleMelanocytesMiceMice, KnockoutMitosisApoptosis Regulatory ProteinsReceptor, Notch1SomatomedinsTumor Suppressor Protein p53

Identifiers

PMID17611229
PMCPMC2583345
OpenAlexW2044168765

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.