Evidence map›Paper›PMID 23595228›Full record

ArticleGenome research2013

NF-Y coassociates with FOS at promoters, enhancers, repetitive elements, and inactive chromatin regions, and is stereo-positioned with growth-controlling transcription factors.

Joseph D Fleming, Giulio Pavesi, Paolo Benatti, Carol Imbriano, Roberto Mantovani, Kevin Struhl

Open access · hybridAbstract read
In one paragraph

Article in Genome research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
–field-weighted citation impact
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

86 citing papers in PubMed, 141 citations in OpenAlex.

  1. Article
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  8. Article
  9. The role(s) of NF-Y in development and differentiation.Cell death and differentiation · 2025
    Review
  10. PhpCNature communications · 2025
    Article
  11. Article
  12. Article
  13. Article
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  15. Article
  16. Review
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26 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Joseph D FlemingDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Giulio Pavesi
Paolo Benatti
Carol Imbriano
Roberto Mantovani
Kevin Struhl
Harvard University · USUniversity of Milan · ITUniversity of Modena and Reggio Emilia · IT

Funding

Production Center for Global Mapping of Regulatory ElementsU54HG004558 · NHGRI · YALE UNIVERSITY · PI SNYDER, MICHAEL P. · 2007 to 2011
$15.4M
MOLECULAR MECHANISMS OF YEAST TRANSCRIPTIONAL INITIATIONR01GM030186 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI STRUHL, KEVIN · 1985 to 2018
$13.6M
MECHANISMS OF YEAST TRANSCRIPTIONAL INITITATIONR37GM030186 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI STRUHL, KEVIN · 1993 to 2002
$2.1M
NHGRI NIH HHS HG4558NHGRI NIH HHS U54 HG004558NIGMS NIH HHS GM30186NIGMS NIH HHS R01 GM030186NIGMS NIH HHS R37 GM030186
6 · The paper itself

Abstract

NF-Y, a trimeric transcription factor (TF) composed of two histone-like subunits (NF-YB and NF-YC) and a sequence-specific subunit (NF-YA), binds to the CCAAT motif, a common promoter element. Genome-wide mapping reveals 5000-15,000 NF-Y binding sites depending on the cell type, with the NF-YA and NF-YB subunits binding asymmetrically with respect to the CCAAT motif. Despite being characterized as a proximal promoter TF, only 25% of NF-Y sites map to promoters. A comparable number of NF-Y sites are located at enhancers, many of which are tissue specific, and nearly half of the NF-Y sites are in select subclasses of HERV LTR repeats. Unlike most TFs, NF-Y can access its target DNA motif in inactive (nonmodified) or polycomb-repressed chromatin domains. Unexpectedly, NF-Y extensively colocalizes with FOS in all genomic contexts, and this often occurs in the absence of JUN and the AP-1 motif. NF-Y also coassociates with a select cluster of growth-controlling and oncogenic TFs, consistent with the abundance of CCAAT motifs in the promoters of genes overexpressed in cancer. Interestingly, NF-Y and several growth-controlling TFs bind in a stereo-specific manner, suggesting a mechanism for cooperative action at promoters and enhancers. Our results indicate that NF-Y is not merely a commonly used proximal promoter TF, but rather performs a more diverse set of biological functions, many of which are likely to involve coassociation with FOS.

Indexed as

Enhancer Elements, GeneticPromoter Regions, GeneticBase SequenceBinding SitesCCAAT-Binding FactorChromatinConsensus SequenceGene Expression RegulationGene OntologyGenome, HumanHeLa CellsHumansK562 CellsMolecular Sequence AnnotationOrgan SpecificityProtein BindingCCAAT-Binding FactorChromatinNFYA protein, humanNFYB protein, humanProto-Oncogene Proteins c-fosTranscription Factors

Identifiers

PMID23595228
PMCPMC3730095
OpenAlexW2144256548

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.