Evidence map›Paper›PMID 9722615›Full record

ArticleThe Journal of cell biology1998

Directed expression of keratin 16 to the progenitor basal cells of transgenic mouse skin delays skin maturation.

R D Paladini, P A Coulombe

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

38 citing papers in PubMed, 80 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Keratin isoform shifts modulate motility signals during wound healing.bioRxiv : the preprint server for biology · 2024
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Interleukin-17A and Keratinocytes in Psoriasis.International journal of molecular sciences · 2020
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Keratin 16 regulates innate immunity in response to epidermal barrier breach.Proceedings of the National Academy of Sciences of the United States of America · 2013
    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

2 authors at 1 institution in 1 country.

R D PaladiniDepartment of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
P A Coulombe
Johns Hopkins University · US

Funding

Non-Canonical Functions of Keratin Proteins in SkinR01AR044232 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COULOMBE, PIERRE · 1996 to 2020
$8.6M
NIAMS NIH HHS AR44232NIAMS NIH HHS R01 AR044232
6 · The paper itself

Abstract

We previously hypothesized that the type I keratin 16 (K16) plays a role in the process of keratinocyte activation that occurs in response to skin injury (Paladini, R.D., K. Takahashi, N.S. Bravo, and P.A. Coulombe. 1996. J. Cell Biol. 132:381-397). To further examine its properties in vivo, the human K16 cDNA was constitutively expressed in the progenitor basal layer of transgenic mouse skin using the K14 gene promoter. Mice that express approximately as much K16 protein as endogenous K14 display a dramatic postnatal phenotype that consists of skin that is hyperkeratotic, scaly, and essentially devoid of fur. Histologically, the epidermis is thickened because of hyperproliferation of transgenic basal cells, whereas the hair follicles are decreased in number, poorly developed, and hypoproliferative. Microscopically, the transgenic keratinocytes are hypertrophic and feature an altered keratin filament network and decreased cell-cell adhesion. The phenotype normalizes at approximately 5 wk after birth. In contrast, control mice expressing a K16-K14 chimeric protein to comparable levels are normal. The character and temporal evolution of the phenotype in the K16 transgenic mice are reminiscent of the activated EGF receptor- mediated signaling pathway in skin. In fact, tyrosine phosphorylation of the EGF receptor is increased in the newborn skin of K16 transgenic mice. We conclude that expression of K16 can significantly alter the response of skin keratinocytes to signaling cues, a distinctive property likely resulting from its unique COOH-terminal tail domain.

Indexed as

AnimalsCell Adhesion MoleculesErbB ReceptorsGene Expression Regulation, DevelopmentalHistocytochemistryHumansImmunohistochemistryKeratin-14KeratinocytesKeratinsMiceMice, TransgenicMicroscopy, ElectronPhenotypePhosphorylationRecombinant Fusion ProteinsCell Adhesion MoleculesErbB ReceptorsKeratin-14KeratinsKRT14 protein, humanKrt14 protein, mouseRecombinant Fusion ProteinsTyrosine

Identifiers

PMID9722615
PMCPMC2132878
OpenAlexW2123194436

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.