Evidence map›Paper›PMID 23569325›Full record

ArticleThe Journal of experimental medicine2013

Coordinated transcriptional regulation of bone homeostasis by Ebf1 and Zfp521 in both mesenchymal and hematopoietic lineages.

Riku Kiviranta, Kei Yamana, Hiroaki Saito, Daniel K Ho, Julius Laine, Kati Tarkkonen, Vappu Nieminen-Pihala, Eric Hesse, Diego Correa, Jorma Määttä and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  8. iScience · 2021
    Article
  9. Article
  10. The ClassicGenetics · 2020
    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

17 authors at 10 institutions in 4 countries.

Riku KivirantaDepartment of Medicine, Massachusetts General Hospital, Harvard University, Boston, MA 02115, USA.
Kei Yamana
Hiroaki Saito
Daniel K Ho
Julius Laine
Kati Tarkkonen
Vappu Nieminen-Pihala
Eric Hesse
Diego Correa
Jorma Määttä
Lino Tessarollo
Evan D Rosen
William C Horne
Nancy A Jenkins
Neal G Copeland
Soren Warming
Roland Baron
Hadassah Medical Center · ILHarvard University · USTurku University Hospital · FICenter for Cancer Research · USHarvard University Press · USHouston Methodist · USMassachusetts General Hospital · USMethodist Hospital · USPediatrics and Genetics · USUniversity of Turku · FI

Funding

Gene Targeting FacilityZICBC011265 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TESSAROLLO, LINO · 2010 to 2025
$8.9M
Regulation of Osteoblast Differentiation by Delta FosBR01AR048218 · NIAMS · YALE UNIVERSITY · PI BARON, ROLAND E · 2002 to 2012
$5.0M
Role of Zfp521 in bone formation and anabolic responsesR01AR057769 · NIAMS · HARVARD MEDICAL SCHOOL · PI BARON, ROLAND E · 2010 to 2014
$3.0M
NIAMS NIH HHS AR048218NIAMS NIH HHS AR57769NIAMS NIH HHS R01 AR048218NIAMS NIH HHS R01 AR057769
6 · The paper itself

Abstract

Bone homeostasis is maintained by the coupled actions of hematopoietic bone-resorbing osteoclasts (OCs) and mesenchymal bone-forming osteoblasts (OBs). Here we identify early B cell factor 1 (Ebf1) and the transcriptional coregulator Zfp521 as components of the machinery that regulates bone homeostasis through coordinated effects in both lineages. Deletion of Zfp521 in OBs led to impaired bone formation and increased OB-dependent osteoclastogenesis (OC-genesis), and deletion in hematopoietic cells revealed a strong cell-autonomous role for Zfp521 in OC progenitors. In adult mice, the effects of Zfp521 were largely caused by repression of Ebf1, and the bone phenotype of Zfp521(+/-) mice was rescued in Zfp521(+/-):Ebf1(+/-) mice. Zfp521 interacted with Ebf1 and repressed its transcriptional activity. Accordingly, deletion of Zfp521 led to increased Ebf1 activity in OBs and OCs. In vivo, Ebf1 overexpression in OBs resulted in suppressed bone formation, similar to the phenotype seen after OB-targeted deletion of Zfp521. Conversely, Ebf1 deletion led to cell-autonomous defects in both OB-dependent and cell-intrinsic OC-genesis, a phenotype opposite to that of the Zfp521 knockout. Thus, we have identified the interplay between Zfp521 and Ebf1 as a novel rheostat for bone homeostasis.

Indexed as

Gene Expression RegulationAnimalsBone and BonesBone Diseases, MetabolicBone ResorptionCell LineageCore Binding Factor Alpha 1 SubunitGene DeletionGerm CellsHaploinsufficiencyHematopoietic SystemHomeostasisMesodermMiceOsteoblastsOsteoclastsCore Binding Factor Alpha 1 SubunitEbf1 protein, mouseEvi3 protein, mouseRunx2 protein, mouseTrans-ActivatorsTranscription Factors

Identifiers

PMID23569325
PMCPMC3646489
OpenAlexW2123661716

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.