Evidence map›Paper›PMID 25425188›Full record

ArticleTranscription2014

Shared transcription factors contribute to distinct cell fates.

Felicia S L Ng, Fernando J Calero-Nieto, Berthold Göttgens

Open access · hybridAbstract read
In one paragraph

Article in Transcription, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 93% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

3 authors at 3 institutions in 3 countries.

Felicia S L Nga Department of Haematology; Wellcome Trust and MRC Cambridge Stem Cell Institute & Cambridge Institute for Medical Research ; Cambridge University ; Cambridge , UK.
Fernando J Calero-Nieto
Berthold Göttgens
Bridge University · SSStem Cell Institute · PAUniversity of Cambridge · GB

Funding

Biotechnology and Biological Sciences Research CouncilCancer Research UK 12765Medical Research Council MC_PC_12009Wellcome Trust
6 · The paper itself

Abstract

Genome-wide transcription factor (TF) binding profiles differ dramatically between cell types. However, not much is known about the relationship between cell-type-specific binding patterns and gene expression. A recent study demonstrated how the same TFs can have functional roles when binding to largely non-overlapping genomic regions in hematopoietic progenitor and mast cells. Cell-type specific binding profiles of shared TFs are therefore not merely the consequence of opportunistic and functionally irrelevant binding to accessible chromatin, but instead have the potential to make meaningful contributions to cell-type specific transcriptional programs.

Indexed as

Gene ExpressionOrgan SpecificityAnimalsCell LineageHumansTranscription FactorsTranscription Factorsbinding motifChIP-seq, ChIP sequencingGAM, generalized additive modelhematopoiesismast cellregression modelRNA-seq, RNA sequencingTF, transcription factor

Identifiers

PMID25425188
PMCPMC4581352
OpenAlexW1998060270

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.