Evidence map›Paper›PMID 7688128›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1993

Epidermal growth factor and transforming growth factor alpha specifically induce the activation- and hyperproliferation-associated keratins 6 and 16.

C K Jiang, T Magnaldo, M Ohtsuki, I M Freedberg, F Bernerd, M Blumenberg

Open access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 189 citations in OpenAlex.

  1. Pooled it
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  15. Mechanisms for Reducing Neuropathic Pain.Molecular neurobiology · 2020
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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 2 institutions in 1 country.

C K JiangRonald O. Perelman Department of Dermatology, New York University Medical Center, NY 10016.
T Magnaldo
M Ohtsuki
I M Freedberg
F Bernerd
M Blumenberg
Columbia University Irving Medical Center · USNew York University · US

Funding

SKIN DISEASES RESEARCH CENTERP30AR039749 · NIAMS · NEW YORK UNIVERSITY · PI BYSTRYN, JEAN-CLAUDE · 1988 to 1993
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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
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NIAMS NIH HHS AR30682NIAMS NIH HHS AR39176NIAMS NIH HHS AR39749
6 · The paper itself

Abstract

Epidermal injury results in activation of keratinocytes which produce and respond to growth factors and cytokines and become migratory. Activated keratinocytes express a specific pair of keratin proteins, K6 and K16, distinct from the keratins in the healthy epidermis. Keratinocytes can be activated, for example, by binding of the appropriate ligands to the epidermal growth factor receptor (EGFR). We have analyzed the effects of EGFR activation on keratin gene transcription by transfecting DNAs containing keratin promoters linked to a reporter gene into primary cultures of human epidermal keratinocytes in the presence or absence of EGF or transforming growth factor alpha (TGF alpha), two growth factors that activate EGFR. The activation of EGFR had no effect on the promoters of simple epithelial, basal-layer-specific, or differentiation-specific keratins. In contrast, the expression of K6 and K16 was strongly and specifically induced. A 20-bp DNA segment of the K16 gene promoter conveyed the EGF regulation, functioned in a heterologous construct, and therefore constituted an EGF-responsive element. A nuclear protein specifically bound to this element and to the analogous sequence of the K6 promoter. Thus, EGF specifically induces K6 and K16, markers of activated keratinocytes, via nuclear proteins that bind to EGF-responsive elements in the promoters of these keratin genes.

Indexed as

Transcription, GeneticBase SequenceCell DivisionChloramphenicol O-AcetyltransferaseDNA-Binding ProteinsEpidermal Growth FactorGene Expression RegulationHumansKeratinocytesKeratinsMolecular Sequence DataMultigene FamilyPromoter Regions, GeneticRecombinant Fusion ProteinsSkinTransfectionChloramphenicol O-AcetyltransferaseDNA-Binding ProteinsEpidermal Growth FactorKeratinsRecombinant Fusion ProteinsTransforming Growth Factor alpha

Identifiers

PMID7688128
PMCPMC47017
OpenAlexW2019720769

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.