Evidence map›Paper›PMID 21473784›Full record

ArticleBMC genomics2011

Nuclear factor I revealed as family of promoter binding transcription activators.

Milos Pjanic, Petar Pjanic, Christoph Schmid, Giovanna Ambrosini, Armelle Gaussin, Genta Plasari, Christian Mazza, Philipp Bucher, Nicolas Mermod

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Epigenetic Causes of Overgrowth Syndromes.The Journal of clinical endocrinology and metabolism · 2024
    Review
  7. NFIXing Cancer: The Role of NFIX in Oxidative Stress Response and Cell Fate.International journal of molecular sciences · 2023
    Review
  8. Cell-specific expression of theFrontiers in molecular biosciences · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

9 authors at 5 institutions in 2 countries.

Milos PjanicInstitute of Biotechnology, University of Lausanne, Lausanne, Switzerland. pjanic.milos@gmail.com
Petar Pjanic
Christoph Schmid
Giovanna Ambrosini
Armelle Gaussin
Genta Plasari
Christian Mazza
Philipp Bucher
Nicolas Mermod
University of Lausanne · CHÉcole Polytechnique Fédérale de Lausanne · CHSIB Swiss Institute of Bioinformatics · CHUniversity of Belgrade · RSUniversity of Fribourg · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMultiplex experimental assays coupled to computational predictions are being increasingly employed for the simultaneous analysis of many specimens at the genome scale, which quickly generates very large amounts of data. However, inferring valuable biological information from the comparisons of very large genomic datasets still represents an enormous challenge.

resultsAs a study model, we chose the NFI/CTF family of mammalian transcription factors and we compared the results obtained from a genome-wide study of its binding sites with chromatin structure assays, gene expression microarray data, and in silico binding site predictions. We found that NFI/CTF family members preferentially bind their DNA target sites when they are located around transcription start sites when compared to control datasets generated from the random subsampling of the complete set of NFI binding sites. NFI proteins preferably associate with the upstream regions of genes that are highly expressed and that are enriched in active chromatin modifications such as H3K4me3 and H3K36me3. We postulate that this is a causal association and that NFI proteins mainly act as activators of transcription. This was documented for one member of the family (NFI-C), which revealed as a more potent gene activator than repressor in global gene expression analysis. Interestingly, we also discovered the association of NFI with the tri-methylation of lysine 9 of histone H3, a chromatin marker previously associated with the protection against silencing of telomeric genes by NFI.

conclusionTaken together, we illustrate approaches that can be taken to analyze large genomic data, and provide evidence that NFI family members may act in conjunction with specific chromatin modifications to activate gene expression.

Indexed as

Promoter Regions, GeneticTranscriptional ActivationAlgorithmsAnimalsCluster AnalysisGene Expression RegulationGenomicsHistonesMethylationMiceMolecular Sequence DataNFI Transcription FactorsOligonucleotide Array Sequence AnalysisProtein BindingTranscription FactorsTranscription Initiation SiteHistonesNFI Transcription FactorsTranscription Factors

Identifiers

PMID21473784
PMCPMC3082249
OpenAlexW2169019243

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.