Evidence map›Paper›PMID 15060141›Full record

ArticleMolecular and cellular biology2004

Thyroid hormones and gamma interferon specifically increase K15 keratin gene transcription.

Nada Radoja, Olivera Stojadinovic, Ahmad Waseem, Marjana Tomic-Canic, Vladana Milisavljevic, Susan Teebor, Miroslav Blumenberg

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

19 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Thyroid diseases and skin autoimmunity.Reviews in endocrine & metabolic disorders · 2018
    Review
  6. Review
  7. Article
  8. Observational
  9. Article
  10. Keratin k15 as a biomarker of epidermal stem cells.International journal of molecular sciences · 2013
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. 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 2 institutions in 2 countries.

Nada RadojaDepartment of Dermatology, New York University School of Medicine, New York, New York 10016, USA.
Olivera Stojadinovic
Ahmad Waseem
Marjana Tomic-Canic
Vladana Milisavljevic
Susan Teebor
Miroslav Blumenberg
New York University · USQueen Mary University of London · GB

Funding

SIGNAL TRANSDUCTION MECHANISMS IN EPIDERMISR01AR041850 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BLUMENBERG, MIROSLAV · 1994 to 2003
$1.1M
GLUCOCORTICOIDS IN EPIDERMIS: MECHANISMS OF ACTIONR01AR045974 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI TOMIC-CANIC, MARJANA · 2000 to 2004
$960k
STUDIES OF EPIDERMAL MACROMOLECULAR METABOLISMR01AR030682 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FREEDBERG, IRWIN M · 1986 to 1999
–
REGULATION OF KERATINIZATION BY HORMONES AND VITAMINSR01AR040522 · NIAMS · NEW YORK UNIVERSITY · PI BLUMENBERG, MIROSLAV · 1992 to 1995
–
NIAMS NIH HHS AR30682NIAMS NIH HHS AR40522NIAMS NIH HHS AR41850NIAMS NIH HHS AR45974NIAMS NIH HHS R01 AR041850NIAMS NIH HHS R01 AR045974
6 · The paper itself

Abstract

Basal layers of stratified epithelia express keratins K5, K14, and K15, which assemble into intermediate filament networks. Mutations in K5 or K14 genes cause epidermolysis bullosa simplex (EBS), a disorder with blistering in the basal layer due to cell fragility. Nonkeratinizing stratified epithelia, e.g., in the esophagus, produce more keratin K15 than epidermis, which alleviates the esophageal symptoms in patients with K14 mutations. Hypothesizing that increasing the cellular content of K15 could compensate for the mutant K14 and thus ease skin blistering in K14 EBS patients, we cloned the promoter of the K15 gene and examined its transcriptional regulation. Using cotransfection, gel mobility shifts, and DNase I footprinting, we have identified the regulators of K15 promoter activity and their binding sites. We focused on those that can be manipulated with extracellular agents, transcription factors C/EBP, AP-1, and NF-kappaB, nuclear receptors for thyroid hormone, retinoic acid, and glucocorticoids, and the cytokine gamma interferon (IFN-gamma). We found that C/EBP-beta and AP-1 induced, while retinoic acid, glucocorticoid receptors, and NF-kappaB suppressed, the K15 promoter, along with other keratin gene promoters. However, the thyroid hormone and IFN-gamma uniquely and potently activated the K15 promoter. Using these agents, we could boost the amounts of K15 in human epidermis. Our findings suggest that treatments based on thyroid hormone and IFN-gamma could become effective agents in therapy for patients with EBS.

Indexed as

Gene Expression RegulationPromoter Regions, GeneticTranscription, GeneticAnimalsBase SequenceCells, CulturedEpidermal CellsEpidermisEpidermolysis BullosaGlucocorticoidsHumansInterferon-gammaKeratin-14Keratin-15KeratinsMolecular Sequence DataGlucocorticoidsInterferon-gammaKeratin-14Keratin-15KeratinsKRT14 protein, humanKRT15 protein, humanReceptors, GlucocorticoidReceptors, Retinoic AcidReceptors, Thyroid HormoneThyroid HormonesTranscription FactorsTretinoin

Identifiers

PMID15060141
PMCPMC381600
OpenAlexW2158042884

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.