Evidence map›Paper›PMID 25527076›Full record

ArticleDevelopmental biology2015

Foxp1/2/4 regulate endochondral ossification as a suppresser complex.

Haixia Zhao, Wenrong Zhou, Zhengju Yao, Yong Wan, Jingjing Cao, Lingling Zhang, Jianzhi Zhao, Hanjun Li, Rujiang Zhou, Baojie Li and 8 more

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

52 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
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    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

18 authors at 6 institutions in 5 countries.

Haixia ZhaoBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, China.
Wenrong ZhouBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, China.
Zhengju YaoBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, China.
Yong WanBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, China.
Jingjing CaoBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, China.
Lingling ZhangBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, China.
Jianzhi ZhaoBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, China.
Hanjun LiBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, China.
Rujiang ZhouBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, China.
Baojie LiBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, China.
Gang WeiShanghai Institutes for Biological Sciences, Chinese Academy of Sciences (CAS), Shanghai 200032, China.
Zhenlin ZhangDepartment of Orthopedic Surgery, Shanghai Jiao Tong University Affiliated the Sixth People׳s Hospital, Shanghai, China.
Catherine A FrenchChampalimaud Neuroscience Programme, Champalimaud Centre for the Unknown, Lisbon, Portugal.
Joseph D DekkerInstitute for Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA.
Yingzi YangDevelopmental Genetics Section, National Human Genome Research Institute, NIH, MD 20892, USA.
Simon E FisherLanguage and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, The Netherlands; Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, The Netherlands.
Haley O TuckerInstitute for Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA.
Xizhi GuoBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, China. Electronic address: xzguo2005@sjtu.edu.cn.
Shanghai Jiao Tong University · CNThe University of Texas at Austin · USChampalimaud Foundation · PTChinese Academy of Sciences · CNNational Human Genome Research Institute · USRadboud University Nijmegen · NL

Funding

Wnt signaling in vetebrate limb and skeletal developmentZIAHG000187 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI YANG, YINGZI · 2009 to 2015
$7.1M
Hedgehog signaling in adult bone and cartilage homeostasisZIAHG200342 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI YANG, YINGZI · 2009 to 2015
$3.1M
MAR MEDIATED GENETIC SWITCH FOR IGH ENHANCER CONTROLR01CA031534 · NCI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI TUCKER, HALEY O · 1985 to 2012
$2.9M
NCI NIH HHS R01 CA031534NCI NIH HHS R01CA31534Wellcome Trust 080971
6 · The paper itself

Abstract

Osteoblast induction and differentiation in developing long bones is dynamically controlled by the opposing action of transcriptional activators and repressors. In contrast to the long list of activators that have been discovered over past decades, the network of repressors is not well-defined. Here we identify the expression of Foxp1/2/4 proteins, comprised of Forkhead-box (Fox) transcription factors of the Foxp subfamily, in both perichondrial skeletal progenitors and proliferating chondrocytes during endochondral ossification. Mice carrying loss-of-function and gain-of-function Foxp mutations had gross defects in appendicular skeleton formation. At the cellular level, over-expression of Foxp1/2/4 in chondroctyes abrogated osteoblast formation and chondrocyte hypertrophy. Conversely, single or compound deficiency of Foxp1/2/4 in skeletal progenitors or chondrocytes resulted in premature osteoblast differentiation in the perichondrium, coupled with impaired proliferation, survival, and hypertrophy of chondrocytes in the growth plate. Foxp1/2/4 and Runx2 proteins interacted in vitro and in vivo, and Foxp1/2/4 repressed Runx2 transactivation function in heterologous cells. This study establishes Foxp1/2/4 proteins as coordinators of osteogenesis and chondrocyte hypertrophy in developing long bones and suggests that a novel transcriptional repressor network involving Foxp1/2/4 may regulate Runx2 during endochondral ossification.

Indexed as

OsteogenesisAnimalsBone and BonesCalcification, PhysiologicChlorocebus aethiopsChondrocytesChondrogenesisCore Binding Factor Alpha 1 SubunitCOS CellsExtremitiesForkhead Transcription FactorsGene DeletionGene Expression Regulation, DevelopmentalHEK293 CellsHumansHypertrophyCore Binding Factor Alpha 1 SubunitCre recombinaseForkhead Transcription FactorsFoxp1 protein, mouseFoxp2 protein, mouseFoxp4 protein, mouseIntegrasesRepressor ProteinsEndochondral ossificationFoxp1Foxp2Foxp4OsteoblastTranscriptional repressor

Identifiers

PMID25527076
PMCPMC4342236
OpenAlexW2164041582

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.