Evidence map›Paper›PMID 10825196›Full record

ArticleMolecular and cellular biology2000

Novel mechanism of steroid action in skin through glucocorticoid receptor monomers.

N Radoja, M Komine, S H Jho, M Blumenberg, M Tomic-Canic

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Anti-Psoriatic Effects of Antimony Compounds In Vitro.Molecules (Basel, Switzerland) · 2021
    Article
  5. Article
  6. Deletion ofFrontiers in cell and developmental biology · 2021
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Mechanisms of action of topical corticosteroids in psoriasis.International journal of endocrinology · 2012
    Article
  17. Article
  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

5 authors at 3 institutions in 3 countries.

N RadojaThe Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, New York 10016, USA.
M Komine
S H Jho
M Blumenberg
M Tomic-Canic
Vienna Institute for Nature Conservation & Analyses · ATThe University of Tokyo · JPUniversity School · US

Funding

STUDIES OF EPIDERMAL MACROMOLECULAR METABOLISMR01AR030682 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FREEDBERG, IRWIN M · 1986 to 1999
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REGULATION OF KERATINIZATION BY HORMONES AND VITAMINSR01AR040522 · NIAMS · NEW YORK UNIVERSITY · PI BLUMENBERG, MIROSLAV · 1992 to 1995
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GENETICS OF INHERITED DISORDERS OF KERATINIZATIONR29AR039176 · NIAMS · NEW YORK UNIVERSITY · PI BLUMENBERG, MIROSLAV · 1988 to 1990
–
NIAMS NIH HHS AR30682BNIAMS NIH HHS AR39176NIAMS NIH HHS AR40522
6 · The paper itself

Abstract

Glucocorticoids (GCs), important regulators of epidermal growth, differentiation, and homeostasis, are used extensively in the treatment of skin diseases. Using keratin gene expression as a paradigm of epidermal physiology and pathology, we have developed a model system to study the molecular mechanism of GCs action in skin. Here we describe a novel mechanism of suppression of transcription by the glucocorticoid receptor (GR) that represents an example of customizing a device for transcriptional regulation to target a specific group of genes within the target tissue, in our case, epidermis. We have shown that GCs repress the expression of the basal-cell-specific keratins K5 and K14 and disease-associated keratins K6, K16, and K17 but not the differentiation-specific keratins K3 and K10 or the simple epithelium-specific keratins K8, K18, and K19. We have identified the negative recognition elements (nGREs) in all five regulated keratin gene promoters. Detailed footprinting revealed that the function of nGREs is to instruct the GR to bind as four monomers. Furthermore, using cotransfection and antisense technology we have found that, unlike SRC-1 and GRIP-1, which are not involved in the GR complex that suppresses keratin genes, histone acetyltransferase and CBP are. In addition, we have found that GR, independently from GREs, blocks the induction of keratin gene expression by AP1. We conclude that GR suppresses keratin gene expression through two independent mechanisms: directly, through interactions of keratin nGREs with four GR monomers, as well as indirectly, by blocking the AP1 induction of keratin gene expression.

Indexed as

Gene Expression RegulationGlucocorticoidsHeLa CellsHumansKeratinocytesKeratinsPromoter Regions, GeneticReceptors, GlucocorticoidSkinSkin DiseasesGlucocorticoidsKeratinsReceptors, Glucocorticoid

Identifiers

PMID10825196
PMCPMC85800
OpenAlexW2056582616

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.