Evidence map›Paper›PMID 7516473›Full record

ArticleMolecular and cellular biology1994

Disease-activated transcription factor: allergic reactions in human skin cause nuclear translocation of STAT-91 and induce synthesis of keratin K17.

C K Jiang, S Flanagan, M Ohtsuki, K Shuai, I M Freedberg, M Blumenberg

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Oral lichen planus: a microbiologist point of view.International microbiology : the official journal of the Spanish Society for Microbiology · 2021
    Review
  5. Article
  6. Effect of Calcipotriol on IFN-γ-Induced Keratin 17 Expression in Immortalized Human Epidermal Keratinocyte Cells.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  7. Article
  8. Article
  9. Overexpression of keratin 17 is associated with poor prognosis in epithelial ovarian cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

C K JiangRonald O. Perelman Department of Dermatology, New York University Medical Center, New York 10016.
S Flanagan
M Ohtsuki
K Shuai
I M Freedberg
M Blumenberg
New York University · US

Funding

SKIN DISEASES RESEARCH CENTERP30AR039749 · NIAMS · NEW YORK UNIVERSITY · PI BYSTRYN, JEAN-CLAUDE · 1988 to 1993
–
STUDIES OF EPIDERMAL MACROMOLECULAR METABOLISMR01AR030682 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FREEDBERG, IRWIN M · 1986 to 1999
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GENETICS OF INHERITED DISORDERS OF KERATINIZATIONR29AR039176 · NIAMS · NEW YORK UNIVERSITY · PI BLUMENBERG, MIROSLAV · 1988 to 1990
–
NIAMS NIH HHS AR30682NIAMS NIH HHS AR39176NIAMS NIH HHS AR39749
6 · The paper itself

Abstract

Epidermal keratinocytes have important immunologic functions, which is apparent during wound healing, in psoriasis, and in allergic and inflammatory reactions. In these processes, keratinocytes not only produce cytokines and growth factors that attract and affect lymphocytes but also respond to the polypeptide factors produced by the lymphocytes. Gamma interferon (IFN-gamma) is one such signaling polypeptide. Its primary molecular effect is activation of specific transcription factors that regulate gene expression in target cells. In this work, we present a molecular mechanism of lymphocyte-keratinocyte signaling in the epidermis. We have induced cutaneous delayed-type hypersensitivity reactions that are associated with an accumulation of lymphocytes. These resulted in activation and nuclear translocation of STAT-91, the IFN-gamma-activated transcription factor, in keratinocytes in vivo and subsequent induction of transcription of keratin K17. Within the promoter of the K17 keratin gene, we have identified and characterized a site that confers the responsiveness to IFN-gamma and that binds the transcription factor STAT-91. Other keratin gene promoters tested were not induced by IFN-gamma. These results characterize at the molecular level a signaling pathway produced by the infiltration of lymphocytes in skin and resulting in the specific alteration of gene expression in keratinocytes.

Indexed as

Promoter Regions, GeneticBase SequenceCell NucleusCloning, MolecularDNA-Binding ProteinsEnhancer Elements, GeneticGene ExpressionHeLa CellsHumansHypersensitivityInterferon-gammaKeratinocytesKeratinsMolecular Sequence DataMutagenesisOligodeoxyribonucleotidesDNA-Binding ProteinsInterferon-gammaKeratinsOligodeoxyribonucleotidesOligonucleotide ProbesSTAT1 protein, humanSTAT1 Transcription FactorTrans-ActivatorsTranscription Factors

Identifiers

PMID7516473
PMCPMC358849
OpenAlexW1895052772

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.