Evidence map›Paper›PMID 11504871›Full record

ArticleNucleic acids research2001

Characterization of Sp1, AP-1, CBF and KRC binding sites and minisatellite DNA as functional elements of the metastasis-associated mts1/S100A4 gene intronic enhancer.

M A Cohn, I Hjelmsø, L C Wu, P Guldberg, E M Lukanidin, E M Tulchinsky

Open access · bronzeAbstract read
In one paragraph

Article in Nucleic acids research, 2001. 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
1.4field-weighted citation impact, top 19% 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, 44 citations in OpenAlex.

  1. Article
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  12. S100A4 and metastasis: a small actor playing many roles.The American journal of pathology · 2010
    Review
  13. Article
  14. Article
  15. Article
  16. Proteins of the S100 family regulate the oligomerization of p53 tumor suppressor.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  17. Article
  18. Article
  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.

M A CohnDepartment of Molecular Cancer Biology, Institute of Cancer Biology, The Danish Cancer Society, Strandboulevarden 49, DK-2100 Copenhagen, Denmark.
I Hjelmsø
L C Wu
P Guldberg
E M Lukanidin
E M Tulchinsky
Danish Cancer Society · DK

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Tasleem J Padamsee · 1985 to 2026
$132.3M
STRUCTURE/FUNCTION OF A MOUSE NF-KB BINDING PROTEINR29GM048798 · NIGMS · OHIO STATE UNIVERSITY · PI WU, LAI-CHU CHU · 1994 to 1998
–
STRUCTURE AND FUNCTION OF A MOUSE NF-KB BINDING PROTEINR55GM048798 · NIGMS · OHIO STATE UNIVERSITY · PI WU, LAI-CHU CHU · 1993 to 1993
–
NCI NIH HHS P30 CA016058NCI NIH HHS P30 CA16058NIGMS NIH HHS GM48798
6 · The paper itself

Abstract

The mts1/S100A4 gene encodes a small acidic calcium-binding protein that is expressed in a cell-specific manner in development, tumorigenesis and certain tissues of adult mice. A composite enhancer that is active in murine mammary adenocarcinoma cells was previously identified in the first intron of the mts1/S100A4 gene. Here we present a detailed analysis of the structure and function of this enhancer in the Mts1/S100A4-expressing CSML100 and non-expressing CSML0 mouse adenocarcinoma cell lines. In CSML100 cells the enhancer activity is composed of at least six cis-elements interacting with Sp1 and AP-1 family members and CBF/AML/PEBP2 and KRC transcription factors. In addition, a minisatellite-like DNA sequence significantly contributes to the enhancer activity via interaction with abundant proteins, which likely have been described previously under the name minisatellite-binding proteins. Extensive mutational analysis of the mts1/S100A4 enhancer revealed a cooperative function of KRC and the factors binding minisatellite DNA. This is the first example of an enhancer where two nuclear factors earlier implicated in different recombination processes cooperate to activate transcription. In Mts1/S100A4-negative CSML0 cells the strength of the enhancer was 7- to 12.5-fold lower compared to that in CSML100 cells, when referred to the activities of three viral promoters. In CSML0 cells the enhancer could be activated by exogenous AP-1 and CBF transcription factors.

Indexed as

Allosteric SiteAnimalsBase SequenceCREB-Binding ProteinDNADNA-Binding ProteinsDNA FootprintingEnhancer Elements, GeneticGene Expression Regulation, NeoplasticGenes, p16Genes, ViralIntronsMiceMinisatellite RepeatsMolecular Sequence DataMutationCREB-Binding ProteinCrebbp protein, mouseDNADNA-Binding ProteinsHivep3 protein, mouseNuclear ProteinsSp1 Transcription FactorTrans-ActivatorsTranscription Factor AP-1Transcription Factors

Identifiers

PMID11504871
PMCPMC55845
OpenAlexW2081065135

What OpenQuestion holds

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Registered trials

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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.