Evidence map›Paper›PMID 7692231›Full record

ArticleMolecular and cellular biology1993

Alu sequence involvement in transcriptional insulation of the keratin 18 gene in transgenic mice.

I S Thorey, G Ceceña, W Reynolds, 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 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.9field-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

21 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Recent advances in transgenic technology.Molecular biotechnology · 1997
    Review
  11. Article
  12. Review
  13. DNA sequence insertion and evolutionary variation in gene regulation.Proceedings of the National Academy of Sciences of the United States of America · 1996
    Review
  14. Article
  15. Article
  16. 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
  17. A tissue-specific promoter that can drive a foreign gene to express in the suprabasal urothelial cells of transgenic mice.Proceedings of the National Academy of Sciences of the United States of America · 1995
    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

4 authors at 1 institution in 1 country.

I S ThoreyCancer Research Center, La Jolla Cancer Research Foundation, California 92037.
G Ceceña
W Reynolds
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 CA 30199NCI NIH HHS CA 42302
6 · The paper itself

Abstract

The human keratin 18 (K18) gene is expressed in a variety of adult simple epithelial tissues, including liver, intestine, lung, and kidney, but is not normally found in skin, muscle, heart, spleen, or most of the brain. Transgenic animals derived from the cloned K18 gene express the transgene in appropriate tissues at levels directly proportional to the copy number and independently of the sites of integration. We have investigated in transgenic mice the dependence of K18 gene expression on the distal 5' and 3' flanking sequences and upon the RNA polymerase III promoter of an Alu repetitive DNA transcription unit immediately upstream of the K18 promoter. Integration site-independent expression of tandemly duplicated K18 transgenes requires the presence of either an 825-bp fragment of the 5' flanking sequence or the 3.5-kb 3' flanking sequence. Mutation of the RNA polymerase III promoter of the Alu element within the 825-bp fragment abolishes copy number-dependent expression in kidney but does not abolish integration site-independent expression when assayed in the absence of the 3' flanking sequence of the K18 gene. The characteristics of integration site-independent expression and copy number-dependent expression are separable. In addition, the formation of the chromatin state of the K18 gene, which likely restricts the tissue-specific expression of this gene, is not dependent upon the distal flanking sequences of the 10-kb K18 gene but rather may depend on internal regulatory regions of the gene.

Indexed as

Repetitive Sequences, Nucleic AcidTranscription, GeneticAnimalsBase SequenceBlotting, NorthernBrainCells, CulturedCloning, MolecularDNA PrimersEndodermExonsFemaleHumansIntestinal MucosaKeratinsKidneyDNA PrimersKeratinsRNA, MessengerRNA Polymerase III

Identifiers

PMID7692231
PMCPMC364737
OpenAlexW2173260753

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.