Evidence map›Paper›PMID 33370256›Full record

ArticlePLoS computational biology2020

On the NF-Y regulome as in ENCODE (2019).

Mirko Ronzio, Andrea Bernardini, Giulio Pavesi, Roberto Mantovani, Diletta Dolfini

Abstract read
In one paragraph

Article in PLoS computational biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Review
  2. Article
  3. Disrupted diencephalon development and neuropeptidergic pathways in zebrafish with autism-risk mutations.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Article
  6. The role(s) of NF-Y in development and differentiation.Cell death and differentiation · 2025
    Review
  7. 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

5 authors.

Mirko RonzioDipartimento di Bioscienze, Università degli Studi di Milano, Milano, Italy.ORCID 0000-0002-4699-4405
Andrea BernardiniDipartimento di Bioscienze, Università degli Studi di Milano, Milano, Italy.
Giulio PavesiDipartimento di Bioscienze, Università degli Studi di Milano, Milano, Italy.
Roberto MantovaniDipartimento di Bioscienze, Università degli Studi di Milano, Milano, Italy.
Diletta DolfiniDipartimento di Bioscienze, Università degli Studi di Milano, Milano, Italy.ORCID 0000-0002-5346-6096

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NF-Y is a trimeric Transcription Factor -TF- which binds with high selectivity to the conserved CCAAT element. Individual ChIP-seq analysis as well as ENCODE have progressively identified locations shared by other TFs. Here, we have analyzed data introduced by ENCODE over the last five years in K562, HeLa-S3 and GM12878, including several chromatin features, as well RNA-seq profiling of HeLa cells after NF-Y inactivation. We double the number of sequence-specific TFs and co-factors reported. We catalogue them in 4 classes based on co-association criteria, infer target genes categorizations, identify positional bias of binding sites and gene expression changes. Larger and novel co-associations emerge, specifically concerning subunits of repressive complexes as well as RNA-binding proteins. On the one hand, these data better define NF-Y association with single members of major classes of TFs, on the other, they suggest that it might have a wider role in the control of mRNA production.

Indexed as

CCAAT-Binding FactorChromatinChromatin ImmunoprecipitationDatasets as TopicHeLa CellsHumansSequence Analysis, RNACCAAT-Binding FactorChromatin

Identifiers

PMID33370256
PMCPMC7793273

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.