Evidence map›Paper›PMID 7680099›Full record

ArticleMolecular and cellular biology1993

cis regulation of the keratin 18 gene in transgenic mice.

N S Neznanov, R G Oshima

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  8. Review
  9. Article
  10. The consensus sequence of a major Alu subfamily contains a functional retinoic acid response element.Proceedings of the National Academy of Sciences of the United States of America · 1995
    Article
  11. Article
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  14. Evolutionary selection against change in many Alu repeat sequences interspersed through primate genomes.Proceedings of the National Academy of Sciences of the United States of America · 1994
    Article
  15. Article
  16. Oncogene activation of human keratin 18 transcription via the Ras signal transduction pathway.Proceedings of the National Academy of Sciences of the United States of America · 1994
    Article
  17. Article
  18. 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.

N S NeznanovCancer Research Center, La Jolla Cancer Research Foundation, California 92037.
R G Oshima
National Foundation for Cancer Research · US

Funding

Tumor Microenvironment and Cancer ImmunologyP30CA030199 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI Michael Jackson · 1985 to 2026
$107.2M
DEVELOPMENTAL CONTROL OF HUMAN CYTOKERATIN EXPRESSIONR01CA042302 · NCI · BURNHAM INSTITUTE FOR MEDICAL RESEARCH · PI OSHIMA, ROBERT G · 1986 to 2002
$1.4M
NCI NIH HHS CA30199NCI NIH HHS CA42302
6 · The paper itself

Abstract

The gene coding for human keratin 18 (K18), a type I intermediate filament protein found in a variety of simple epithelia, is regulated correctly in transgenic mice but is promiscuously expressed after direct transfection into cell culture lines. We have begun an investigation of the mechanisms responsible for the correct regulation of K18 with a comparison of the chromatin state of K18 in permissive and nonpermissive transgenic mouse tissues to identify seven expression-specific, DNase-hypersensitive sites that correlate with known or potential regulatory regions of the gene. Four of these sites are associated with the proximal promoter region and the first intron that has been implicated previously in the transcriptional control of K18. Two hypersensitive sites are associated with a conserved Alu repetitive sequence located immediately upstream of the proximal promoter elements. Transcription of this Alu element in a direction opposite that of K18 was correlated with K18 expression in transgenic tissues. The final hypersensitive site was mapped to exon 6. The potential importance of this region for the expression of K18 was supported by the results of transient expression of the gene and various deleted constructions. In addition, exon 6 and the intron 1 regulatory region were distinguished from the remainder of K18 by differential DNA methylation in expressing and nonexpressing tissues. The CpG-rich proximal promoter and first exon regions remain unmethylated in both permissive and nonpermissive tissues. These results suggest that DNA methylation is not the primary mechanism of control of the gene. An Alu RNA polymerase III transcription unit and exon 6 are implicated in regulation of K18.

Indexed as

Transcription, GeneticAmino Acid SequenceAnimalsBase SequenceCells, CulturedChromatinChromosome MappingDeoxyribonucleasesDNADNA Modification MethylasesDNA, RecombinantExonsHumansKeratinsMethylationMiceChromatinDeoxyribonucleasesDNADNA Modification MethylasesDNA, RecombinantKeratinsRNARNA Polymerase III

Identifiers

PMID7680099
PMCPMC359494
OpenAlexW1833900490

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.