Evidence map›Paper›PMID 24760698›Full record

ArticleThe EMBO journal2014

Key regulators control distinct transcriptional programmes in blood progenitor and mast cells.

Fernando J Calero-Nieto, Felicia S Ng, Nicola K Wilson, Rebecca Hannah, Victoria Moignard, Ana I Leal-Cervantes, Isabel Jimenez-Madrid, Evangelia Diamanti, Lorenz Wernisch, Berthold Göttgens

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 73 citations in OpenAlex.

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  13. How "Neuronal" Are Human Skin Mast Cells?International journal of molecular sciences · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Fernando J Calero-NietoDepartment of Haematology, Wellcome Trust and MRC Cambridge Stem Cell Institute, Cambridge Institute for Medical Research, Cambridge University, Cambridge, UK fjc28@cam.ac.uk bg200@cam.ac.uk.
Felicia S NgDepartment of Haematology, Wellcome Trust and MRC Cambridge Stem Cell Institute, Cambridge Institute for Medical Research, Cambridge University, Cambridge, UK.
Nicola K WilsonDepartment of Haematology, Wellcome Trust and MRC Cambridge Stem Cell Institute, Cambridge Institute for Medical Research, Cambridge University, Cambridge, UK.
Rebecca HannahDepartment of Haematology, Wellcome Trust and MRC Cambridge Stem Cell Institute, Cambridge Institute for Medical Research, Cambridge University, Cambridge, UK.
Victoria MoignardDepartment of Haematology, Wellcome Trust and MRC Cambridge Stem Cell Institute, Cambridge Institute for Medical Research, Cambridge University, Cambridge, UK.
Ana I Leal-CervantesDepartment of Haematology, Wellcome Trust and MRC Cambridge Stem Cell Institute, Cambridge Institute for Medical Research, Cambridge University, Cambridge, UK.
Isabel Jimenez-MadridDepartment of Haematology, Wellcome Trust and MRC Cambridge Stem Cell Institute, Cambridge Institute for Medical Research, Cambridge University, Cambridge, UK.
Evangelia DiamantiDepartment of Haematology, Wellcome Trust and MRC Cambridge Stem Cell Institute, Cambridge Institute for Medical Research, Cambridge University, Cambridge, UK.
Lorenz WernischMRC Biostatistics Unit, Institute of Public Health, Cambridge, UK.
Berthold GöttgensDepartment of Haematology, Wellcome Trust and MRC Cambridge Stem Cell Institute, Cambridge Institute for Medical Research, Cambridge University, Cambridge, UK fjc28@cam.ac.uk bg200@cam.ac.uk.
Wellcome/MRC Cambridge Stem Cell Institute · GBUniversity of Cambridge · GBMRC Biostatistics Unit · GB

Funding

Biotechnology and Biological Sciences Research Council BBS/B/1454XCancer Research UK 12765Medical Research Council G0900951Medical Research Council MC_PC_12009Medical Research Council MC_U105260799National Centre for the Replacement, Refinement and Reduction of Animals in Research G0900729/1Wellcome Trust
6 · The paper itself

Abstract

Despite major advances in the generation of genome-wide binding maps, the mechanisms by which transcription factors (TFs) regulate cell type identity have remained largely obscure. Through comparative analysis of 10 key haematopoietic TFs in both mast cells and blood progenitors, we demonstrate that the largely cell type-specific binding profiles are not opportunistic, but instead contribute to cell type-specific transcriptional control, because (i) mathematical modelling of differential binding of shared TFs can explain differential gene expression, (ii) consensus binding sites are important for cell type-specific binding and (iii) knock-down of blood stem cell regulators in mast cells reveals mast cell-specific genes as direct targets. Finally, we show that the known mast cell regulators Mitf and c-fos likely contribute to the global reorganisation of TF binding profiles. Taken together therefore, our study elucidates how key regulatory TFs contribute to transcriptional programmes in several distinct mammalian cell types.

Indexed as

AnimalsCell LineGene Expression ProfilingGene Expression RegulationGenes, ReporterGenome-Wide Association StudyHematopoiesisMast CellsMiceModels, StatisticalNucleotide MotifsOligonucleotide Array Sequence AnalysisSequence Analysis, DNASequence Analysis, RNAStem CellsTranscription FactorsTranscription Factorsgene regulationhaematopoiesismast cellsprogenitors

Identifiers

PMID24760698
PMCPMC4168288
OpenAlexW2007000447

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.