Evidence map›Paper›PMID 24144697›Full record

ArticleJournal of cell science2013

TAK1 regulates SOX9 expression in chondrocytes and is essential for postnatal development of the growth plate and articular cartilages.

Lin Gao, Tzong-jen Sheu, Yufeng Dong, Donna M Hoak, Michael J Zuscik, Edward M Schwarz, Matthew J Hilton, Regis J O'Keefe, Jennifer H Jonason

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. miR-433 targets BMP and Indian hedgehog signaling to coordinate murine postnatal growth plate dynamics.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026
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  17. Inactivation of Nell-1 in Chondrocytes Significantly Impedes Appendicular Skeletogenesis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019
    Article
  18. Article
  19. SPOP promotes ATF2 ubiquitination and degradation to suppress prostate cancer progression.Journal of experimental & clinical cancer research : CR · 2018
    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

9 authors at 1 institution in 1 country.

Lin GaoDepartment of Orthopaedics and Rehabilitation, Center for Musculoskeletal Research, University of Rochester, Rochester, NY, USA.
Tzong-jen Sheu
Yufeng Dong
Donna M Hoak
Michael J Zuscik
Edward M Schwarz
Matthew J Hilton
Regis J O'Keefe
Jennifer H Jonason
University of Rochester · US

Funding

Translating PTH Therapy as an Adjuvant for Structural AllograftingP50AR054041 · NIAMS · UNIVERSITY OF ROCHESTER · PI O'KEEFE, REGIS J · 2006 to 2016
$15.7M
Notch Signaling in Joint Cartilage Maintenance and ArthritisR01AR063071 · NIAMS · UNIVERSITY OF ROCHESTER · PI HILTON, MATTHEW J. · 2012 to 2021
$3.9M
The University of Rochester Core Center for Musculoskeletal Biology and MedicineP30AR061307 · NIAMS · UNIVERSITY OF ROCHESTER · PI SCHWARZ, EDWARD M. · 2011 to 2015
$3.0M
Notch Signaling in Cartilage DevelopmentR01AR057022 · NIAMS · UNIVERSITY OF ROCHESTER · PI HILTON, MATTHEW J. · 2010 to 2014
$1.7M
The use of genetic models to define the role of beta-catenin in post-natal growthR01AR053717 · NIAMS · UNIVERSITY OF ROCHESTER · PI O'KEEFE, REGIS J · 2007 to 2011
$1.6M
NIAMS NIH HHS P30 AR061307NIAMS NIH HHS P50 AR054041NIAMS NIH HHS R01 AR053717NIAMS NIH HHS R01 AR057022NIAMS NIH HHS R01 AR063071
6 · The paper itself

Abstract

TAK1 is a MAP3K that mediates non-canonical TGF-β and BMP signaling. During the embryonic period, TAK1 is essential for cartilage and joint development as deletion of Tak1 in chondro-osteo progenitor cells leads to severe chondrodysplasia with defects in both chondrocyte proliferation and maturation. We have investigated the role of TAK1 in committed chondrocytes during early postnatal development. Using the Col2a1-CreER(T2); Tak1(f/f) mouse model, we induced deletion of Tak1 at postnatal day 7 and characterized the skeletal phenotypes of these mice at 1 and 3 months of age. Mice with chondrocyte-specific Tak1 deletion exhibited severe growth retardation and reduced proteoglycan and type II collagen content in the extracellular matrix of the articular cartilage. We found reduced Col2a1 and Acan expression, but increased Mmp13 and Adamts5 expression, in Tak1-deficient chondrocytes along with reduced expression of the SOX trio of transcription factors, SOX9, SOX5 and SOX6. In vitro, BMP2 stimulated Sox9 gene expression and Sox9 promoter activity. These effects were reduced; however, following Tak1 deletion or treatment with a TAK1 kinase inhibitor. TAK1 affects both canonical and non-canonical BMP signal transduction and we found that both of these pathways contribute to BMP2-mediated Sox9 promoter activation. Additionally, we found that ATF2 directly binds the Sox9 promoter in response to BMP signaling and that this effect is dependent upon TAK1 kinase activity. These novel findings establish that TAK1 contributes to BMP2-mediated Sox9 gene expression and is essential for the postnatal development of normal growth plate and articular cartilages.

Indexed as

Activating Transcription Factor 2AnimalsBone Morphogenetic Protein 2Cartilage, ArticularCell ProliferationCells, CulturedChondrocytesExtracellular MatrixGene DeletionGene Expression RegulationGrowth PlateMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMiceMice, TransgenicPromoter Regions, GeneticActivating Transcription Factor 2Atf2 protein, mouseBmp2 protein, mouseBone Morphogenetic Protein 2MAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesProteoglycansSox9 protein, mouseSOX9 Transcription FactorATF2CartilageChondrocyteSOX9TAK1

Identifiers

PMID24144697
PMCPMC3860312
OpenAlexW2136823472

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.