Evidence map›Paper›PMID 20543837›Full record

ArticleNature immunology2010

A global network of transcription factors, involving E2A, EBF1 and Foxo1, that orchestrates B cell fate.

Yin C Lin, Suchit Jhunjhunwala, Christopher Benner, Sven Heinz, Eva Welinder, Robert Mansson, Mikael Sigvardsson, James Hagman, Celso A Espinoza, Janusz Dutkowski and 3 more

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 331 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
331citing papers in PubMed, 1 pooled it
20.3field-weighted citation impact, top 1% 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

331 citing papers in PubMed, 1 synthesis or guideline pooled it, 507 citations in OpenAlex.

  1. Pooled it
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271 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 2 countries.

Yin C LinDepartment of Molecular Biology, University of California, San Diego, La Jolla, California, USA.
Suchit Jhunjhunwala
Christopher Benner
Sven Heinz
Eva Welinder
Robert Mansson
Mikael Sigvardsson
James Hagman
Celso A Espinoza
Janusz Dutkowski
Trey Ideker
Christopher K Glass
Cornelis Murre
University of California, San Diego · USLinköping University · SELudwig Cancer Research · USLund University · SEUniversity of Colorado Denver · US

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PETER J TONTONOZ · 2003 to 2026
$40.4M
Transcriptional Genomics CoreP01DK074868 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASS, CHRISTOPHER K · 2007 to 2016
$16.6M
E2A as a Tumor SuppressorR01CA078384 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MURRE, CORNELIS · 1999 to 2013
$5.4M
The 3D-Structures of the Immunoglobulin Heavy Chain LocusR01AI082850 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MURRE, CORNELIS · 2009 to 2024
$5.4M
TRANSCRIPTIONAL COREGULATORS AND MYELOID GENE EXPRESSIONR01CA052599 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASS, CHRISTOPHER K · 1991 to 2010
$4.6M
E PROTEIN AND B CELL DIFFERENTIATIONR37CA054198 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MURRE, CORNELIS · 2001 to 2008
$3.5M
Function and Regulation of Early B Cell Factor (EBF)R01AI054661 · NIAID · NATIONAL JEWISH HEALTH · PI HAGMAN, JAMES R. · 2004 to 2011
$2.9M
The role of E-proteins in B cell developmentR01CA054198 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MURRE, CORNELIS · 1991 to 2013
$2.2M
Regulation of B Cell Identity and Lineage ProgressionR01AI081878 · NIAID · NATIONAL JEWISH HEALTH · PI HAGMAN, JAMES R. · 2010 to 2014
$1.9M
The Molecular Mechanism for E2A Tumor SuppressorF32CA130276 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LIN, YIN CHUN · 2007 to 2009
$154k
Molecular and genetic analysis of DP103F32HL083752 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HEINZ, SVEN W · 2006 to 2008
$102k
NCI NIH HHS 1F32CA130276NCI NIH HHS CA054198-20NCI NIH HHS CA52599NCI NIH HHS F32 CA130276NCI NIH HHS R01 CA052599NCI NIH HHS R01 CA054198NCI NIH HHS R01 CA078384NCI NIH HHS R37 CA054198NHLBI NIH HHS F32 HL083752NHLBI NIH HHS F32HL083752NIAID NIH HHS AI05466NIAID NIH HHS R01 AI054661NIAID NIH HHS R01 AI081878NIAID NIH HHS R01 AI082850NIDDK NIH HHS DK063491NIDDK NIH HHS P01 DK074868NIDDK NIH HHS P01DK074868NIDDK NIH HHS P30 DK063491
6 · The paper itself

Abstract

It is now established that the transcription factors E2A, EBF1 and Foxo1 have critical roles in B cell development. Here we show that E2A and EBF1 bound regulatory elements present in the Foxo1 locus. E2A and EBF1, as well as E2A and Foxo1, in turn, were wired together by a vast spectrum of cis-regulatory sequences. These associations were dynamic during developmental progression. Occupancy by the E2A isoform E47 directly resulted in greater abundance, as well as a pattern of monomethylation of histone H3 at lysine 4 (H3K4) across putative enhancer regions. Finally, we divided the pro-B cell epigenome into clusters of loci with occupancy by E2A, EBF and Foxo1. From this analysis we constructed a global network consisting of transcriptional regulators, signaling and survival factors that we propose orchestrates B cell fate.

Indexed as

Gene Regulatory NetworksAnimalsBasic Helix-Loop-Helix ProteinsB-LymphocytesCell LineageCells, CulturedForkhead Box Protein O1Forkhead Transcription FactorsGene Expression Regulation, DevelopmentalHistonesLymphopoiesisMethylationMiceMice, Inbred C57BLMice, KnockoutPrecursor Cells, B-LymphoidBasic Helix-Loop-Helix ProteinsEbf1 protein, mouseForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, mouseHistonesTcf3 protein, mouseTcf7l1 protein, mouseTCF Transcription FactorsTrans-ActivatorsTranscription Factor 7-Like 1 Protein

Identifiers

PMID20543837
PMCPMC2896911
OpenAlexW2166773843

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.