Evidence map›Paper›PMID 16128003›Full record

ArticleGene expression2005

NF-Y behaves as a bifunctional transcription factor that can stimulate or repress the FGF-4 promoter in an enhancer-dependent manner.

Cory T Bernadt, Tamara Nowling, Matthew S Wiebe, Angie Rizzino

Open access · hybridAbstract read
In one paragraph

Article in Gene expression, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Identification and Functional Characterization of Novel Genetic Variations in the OCTN1 Promoter.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2014
    Article
  6. Article
  7. Article
  8. Rapid activation of the bivalent gene Sox21 requires displacement of multiple layers of gene-silencing machinery.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011
    Article
  9. Article
  10. 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.

Cory T BernadtEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE 68198-6805, USA.
Tamara Nowling
Matthew S Wiebe
Angie Rizzino
University of Nebraska Medical Center · US

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Steven H Caplan · 1985 to 2026
$55.0M
REGULATION OF GROWTH FACTORS AND EMBRYOGENESISR01CA074771 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI RIZZINO, ARNOLD ANGIE · 1997 to 2005
$1.5M
NCI NIH HHS CA36727NCI NIH HHS CA74771NCI NIH HHS P30 CA036727NCI NIH HHS R01 CA074771
6 · The paper itself

Abstract

NF-Y is a bifunctional transcription factor capable of activating or repressing transcription. NF-Y specifically recognizes CCAAT box motifs present in many eukaryotic promoters. The mechanisms involved in regulating its activity are poorly understood. Previous studies have shown that the FGF-4 promoter is regulated positively by its CCAAT box and NF-Y in embryonal carcinoma (EC) cells where the distal enhancer of the FGF-4 gene is active. Here, we demonstrate that the CCAAT box functions as a negative cis-regulatory element when cis-regulatory elements of the FGF-4 enhancer are disrupted, or after EC cells differentiate and the FGF-4 enhancer is inactivated. We also demonstrate that NF-Y mediates the repression of the CCAAT box and that NF-Y associates with the endogenous FGF-4 gene in both EC cells and EC-differentiated cells. Importantly, we also determined that the orientation and the position of the CCAAT box are critical for its role in regulating the FGF-4 promoter. Together, these studies demonstrate that the distal enhancer of the FGF-4 gene determines whether the CCAAT box of the FGF-4 promoter functions as a positive or a negative cis-regulatory element. In addition, these studies are consistent with NF-Y playing an architectural role in its regulation of the FGF-4 promoter.

Indexed as

Enhancer Elements, GeneticGene Expression Regulation, NeoplasticPromoter Regions, GeneticAnimalsCarcinoma, EmbryonalCCAAT-Binding FactorCell DifferentiationChromatin ImmunoprecipitationFibroblast Growth Factor 4Gene Expression RegulationGenes, ReporterImmunoprecipitationMiceModels, GeneticPlasmidsRegulatory Sequences, Nucleic AcidCCAAT-Binding FactorFGF4 protein, humanFibroblast Growth Factor 4Transcription Factors

Identifiers

PMID16128003
PMCPMC6009113
OpenAlexW2091801017

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.