Evidence map›Paper›PMID 18397998›Full record

ArticleJournal of cell science2008

Inhibition of beta-catenin signaling causes defects in postnatal cartilage development.

Mo Chen, Mei Zhu, Hani Awad, Tian-Fang Li, Tzong-Jen Sheu, Brendan F Boyce, Di Chen, Regis J O'Keefe

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

76 citing papers in PubMed, 132 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Osteolectin increases bone elongation and body length by promoting growth plate chondrocyte proliferation.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  6. Article
  7. Wnt signalling in the articular cartilage: A matter of balance.International journal of experimental pathology · 2023
    Review
  8. Review
  9. Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023
    Review
  10. Review
  11. Regulatory Mechanisms ofInternational journal of molecular sciences · 2022
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. MiR-181a TargetsFrontiers in cell and developmental biology · 2021
    Article
  17. Review
  18. Article
  19. Article
  20. Review

16 more citing papers are in PubMed but not listed here.

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

8 authors at 1 institution in 1 country.

Mo ChenDepartment of Orthopaedics, Center for Musculoskeletal Research, University of Rochester School of Medicine, Rochester, NY 14642, USA.
Mei Zhu
Hani Awad
Tian-Fang Li
Tzong-Jen Sheu
Brendan F Boyce
Di Chen
Regis J O'Keefe
University of Rochester · US

Funding

The Mechanism through which TGF-Beta Maintains Chondrocytes in Proliferating StagR01AR054465 · NIAMS · UNIVERSITY OF ROCHESTER · PI CHEN, DI · 2007 to 2018
$2.7M
GROWTH FACTORS AND EPIPHYSEAL CHONDROCYTE MATURATIONR01AR038945 · NIAMS · UNIVERSITY OF ROCHESTER · PI O'KEEFE, REGIS J. · 1994 to 2006
$2.4M
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
Roles of Smurf1 in Cbfa1 Degradation and Bone FormationR01AR051189 · NIAMS · UNIVERSITY OF ROCHESTER · PI CHEN, DI · 2004 to 2008
$1.5M
Proteasomal Regulation of BMP Signaling in Bone CellsK02AR052411 · NIAMS · UNIVERSITY OF ROCHESTER · PI CHEN, DI · 2006 to 2008
$301k
GROWTH FACTORS AND EPIPHYSEAL CHONDROCYTE MATURATIONR29AR038945 · NIAMS · UNIVERSITY OF ROCHESTER · PI ROSIER, RANDY N · 1987 to 1991
–
NIAMS NIH HHS AR 038945NIAMS NIH HHS AR 053717NIAMS NIH HHS AR 054465NIAMS NIH HHS K02 AR052411NIAMS NIH HHS R01 AR038945NIAMS NIH HHS R01 AR051189NIAMS NIH HHS R01 AR053717NIAMS NIH HHS R01 AR054465
6 · The paper itself

Abstract

The Wnt/beta-catenin signaling pathway is essential for normal skeletal development because conditional gain or loss of function of beta-catenin in cartilage results in embryonic or early postnatal death. To address the role of beta-catenin in postnatal skeletal growth and development, Col2a1-ICAT transgenic mice were generated. Mice were viable and had normal size at birth, but became progressively runted. Transgene expression was limited to the chondrocytes in the growth plate and articular cartilages and was associated with decreased beta-catenin signaling. Col2a1-ICAT transgenic mice showed reduced chondrocyte proliferation and differentiation, and an increase in chondrocyte apoptosis, leading to decreased widths of the proliferating and hypertrophic zones, delayed formation of the secondary ossification center, and reduced skeletal growth. Isolated primary Col2a1-ICAT transgenic chondrocytes showed reduced expression of chondrocyte genes associated with maturation, and demonstrated that VEGF gene expression requires cooperative interactions between BMP2 and beta-catenin signaling. Altogether the findings confirm a crucial role for Wnt/beta-catenin in postnatal growth.

Indexed as

ChondrogenesisSignal TransductionAdaptor Proteins, Signal TransducingAnimalsAnimals, Newbornbeta CateninBone DevelopmentBone Morphogenetic Protein 2Bone Morphogenetic ProteinsCartilageCell Cycle ProteinsCell DifferentiationCell ProliferationChondrocytesEmbryo, MammalianGene Expression Regulation, DevelopmentalAdaptor Proteins, Signal Transducingbeta CateninBmp2 protein, mouseBone Morphogenetic Protein 2Bone Morphogenetic ProteinsCell Cycle ProteinsCtnnbip1 protein, mouseRepressor ProteinsTranscription FactorsTransforming Growth Factor betaVascular Endothelial Growth Factor AWnt Proteins

Identifiers

PMID18397998
PMCPMC2636704
OpenAlexW2137854259

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.