Evidence map›Paper›PMID 18083923›Full record

ArticleAnnals of the New York Academy of Sciences2007

Axin1 and Axin2 are regulated by TGF- and mediate cross-talk between TGF- and Wnt signaling pathways.

Debbie Y Dao, Xue Yang, Di Chen, Michael Zuscik, Regis J O'Keefe

Open access · greenAbstract read
In one paragraph

Article in Annals of the New York Academy of Sciences, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
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  18. WNT Signalling in Osteoarthritis and Its Pharmacological Targeting.Handbook of experimental pharmacology · 2021
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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

5 authors at 1 institution in 1 country.

Debbie Y DaoDepartment of Orthopaedics, Center for Musculoskeletal Research University of Rochester School of Medicine, Rochester, NY 14642, USA.
Xue Yang
Di Chen
Michael Zuscik
Regis J O'Keefe
University of Rochester · US

Funding

Cyclooxygenases in Skeletal RepairR01AR048681 · NIAMS · UNIVERSITY OF ROCHESTER · PI O'KEEFE, REGIS J, ZHANG, XINPING · 2003 to 2013
$3.3M
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
BMP Receptor Signaling and Bone RemodelingR03AR048920 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI CHEN, DI · 2003 to 2005
$234k
NIAMS NIH HHS AR048681NIAMS NIH HHS AR053717NIAMS NIH HHS K02 AR052411NIAMS NIH HHS R01 AR048681NIAMS NIH HHS R01 AR051189NIAMS NIH HHS R01 AR053717NIAMS NIH HHS R03 AR048920
6 · The paper itself

Abstract

Chondrocyte maturation during endochondral bone formation is regulated by a number of signals that either promote or inhibit maturation. Among these, two well-studied signaling pathways play crucial roles in modulating chondrocyte maturation: transforming growth factor-beta (TGF-beta)/Smad3 signaling slows the rate of chondrocyte maturation, while Wingless/INT-1-related (Wnt)/beta-catenin signaling enhances the rate of chondrocyte maturation. Axin1 and Axin2 are functionally equivalent and have been shown to inhibit Wnt/beta-catenin signaling and stimulate TGF-beta signaling. Here we show that while Wnt3a stimulates Axin2 in a negative feedback loop, TGF-beta suppresses the expression of both Axin1 and Axin2 and stimulates beta-catenin signaling. In Axin2 -/- chondrocytes, TGF-beta treatment results in a sustained increase in beta-catenin levels compared to wild-type chondrocytes. In contrast, overexpression of Axin enhanced TGF-beta signaling while overexpression of beta-catenin inhibited the ability of TGF-beta to induce Smad3-sensitive reporters. Finally, the suppression of the Axins is Smad3-dependent since the effect is absent in Smad3 -/- chondrocytes. Altogether these findings show that the Axins act to integrate signals between the Wnt/beta-catenin and TGF-beta/Smad pathways. Since the suppression Axin1 and Axin2 expression by TGF-beta reduces TGF-beta signaling and enhances Wnt/beta-catenin signaling, the overall effect is a shift from TGF-beta toward Wnt/beta-catenin signaling and an acceleration of chondrocyte maturation.

Indexed as

Signal TransductionAnimalsAxin ProteinBase Sequencebeta CateninChondrocytesCytoskeletal ProteinsDNA PrimersGene Expression RegulationMiceRepressor ProteinsReverse Transcriptase Polymerase Chain ReactionTransforming Growth Factor betaWnt ProteinsAxin2 protein, mouseAxin Proteinbeta CateninCytoskeletal ProteinsDNA PrimersRepressor ProteinsTransforming Growth Factor betaWnt Proteins

Identifiers

PMID18083923
PMCPMC2647987
OpenAlexW2144545798

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.