Evidence map›Paper›PMID 21469119›Full record

ArticleEuropean journal of immunology2011

A dose-dependent role for EBF1 in repressing non-B-cell-specific genes.

Kara Lukin, Scott Fields, Lisa Guerrettaz, Desiree Straign, Valerie Rodriguez, Sasan Zandi, Robert Månsson, John C Cambier, Mikael Sigvardsson, James Hagman

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  9. A NovelFrontiers in genetics · 2021
    Article
  10. Article
  11. De Novo Mutations in EBF3 Cause a Neurodevelopmental Syndrome.American journal of human genetics · 2017
    Article
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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

10 authors at 4 institutions in 2 countries.

Kara LukinIntegrated Department of Immunology, National Jewish Health, Denver, CO 80206, USA.
Scott Fields
Lisa Guerrettaz
Desiree Straign
Valerie Rodriguez
Sasan Zandi
Robert Månsson
John C Cambier
Mikael Sigvardsson
James Hagman
University of Colorado Denver · USNational Jewish Health · USLinköping University · SELund University · SE

Funding

THE REGULATION OF V ALPHA 7 EXPRESSING T CELLSP01AI022295 · NIAID · NATIONAL JEWISH HEALTH · PI REFAELI, YOSEF · 1985 to 2011
$11.7M
TRAINING PROGRAM IN IMMUNOLOGYT32AI007405 · NIAID · UNIVERSITY OF COLORADO DENVER · PI Laurel L Lenz, Raul Martin Torres · 1991 to 2026
$10.5M
Colorado Program in Aging and CancerP20CA103680 · NCI · UNIVERSITY OF COLORADO DENVER · PI BYERS, TIM E · 2003 to 2007
$3.2M
Function and Regulation of Early B Cell Factor (EBF)R01AI054661 · NIAID · NATIONAL JEWISH HEALTH · PI HAGMAN, JAMES R. · 2004 to 2011
$2.9M
Regulation of B Cell Identity and Lineage ProgressionR01AI081878 · NIAID · NATIONAL JEWISH HEALTH · PI HAGMAN, JAMES R. · 2010 to 2014
$1.9M
NCI NIH HHS P20 CA103680NCI NIH HHS P20 CA103680-05NIAID NIH HHS 5 T32 AI007405NIAID NIH HHS P01 AI022295NIAID NIH HHS P01 AI22295NIAID NIH HHS R01 AI054661NIAID NIH HHS R01 AI081878NIAID NIH HHS R01 AI54661NIAID NIH HHS R01 AI81878NIAID NIH HHS T32 AI007405
6 · The paper itself

Abstract

In the absence of early B-cell factor 1 (EBF1), B-cell development is arrested at an uncommitted progenitor stage that exhibits increased lineage potentials. Previously, we investigated the roles of EBF1 and its DNA-binding partner Runx1 by evaluating B lymphopoiesis in single (EBF1(het) and Runx1(het)) and compound haploinsufficent (Ebf1(+/-) Runx1(+/-), ER(het)) mice. Here, we demonstrate that decreased Ebf1 gene dosage results in the inappropriate expression of NK-cell lineage-specific genes in B-cell progenitors. Moreover, prolonged expression of Ly6a/Sca-1 suggested the maintenance of a relatively undifferentiated phenotype. These effects were exacerbated by reduced expression of Runx1 and occurred despite expression of Pax5. Repression of inappropriately expressed genes was restored in most pre-B and all immature B cells of ER(het) mice. Enforced EBF1 expression repressed promiscuous transcription in pro-B cells of ER(het) mice and in Ebf1(-/-) Pax5(-/-) fetal liver cells. Together, our studies suggest that normal levels of EBF1 are critical for maintaining B-cell identity by directing repression of non-B-cell-specific genes.

Indexed as

Cell LineageLymphopoiesisAnimalsAntigens, DifferentiationAntigens, LyB-LymphocytesCells, CulturedGene DosageKiller Cells, NaturalMembrane ProteinsMiceMice, KnockoutMice, Mutant StrainsPAX5 Transcription FactorPrecursor Cells, B-LymphoidTrans-ActivatorsAntigens, DifferentiationAntigens, LyEbf1 protein, mouseLy6a protein, mouseMembrane ProteinsPax5 protein, mousePAX5 Transcription FactorTrans-Activators

Identifiers

PMID21469119
PMCPMC3127254
OpenAlexW2086080529

What OpenQuestion holds

Textmetadata
LicenceTDM
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.