Evidence map›Paper›PMID 19047045›Full record

ArticleThe Journal of biological chemistry2009

Sox9 inhibits Wnt signaling by promoting beta-catenin phosphorylation in the nucleus.

Lilia Topol, Wen Chen, Hai Song, Timothy F Day, Yingzi Yang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

124 citing papers in PubMed, 227 citations in OpenAlex.

  1. Article
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  9. Review
  10. Detailed survey of aniScience · 2024
    Article
  11. Article
  12. Article
  13. Wnt signaling in periodontitis.Clinical oral investigations · 2023
    Article
  14. Article
  15. Review
  16. Review
  17. Hypomorphic and dominant-negative impact of truncated SOX9 dysregulates Hedgehog-Wnt signaling, causing campomelia.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  18. Review
  19. MPSI Manifestations and Treatment Outcome: Skeletal Focus.International journal of molecular sciences · 2022
    Review
  20. Article

64 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

5 authors at 2 institutions in 1 country.

Lilia TopolGenetics Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892.
Wen ChenGenetics Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892.
Hai SongGenetics Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892.
Timothy F DayGenetics Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892.
Yingzi YangGenetics Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892. Electronic address: yingzi@mail.nih.gov.
National Institutes of Health · USNational Human Genome Research Institute · US

Funding

Wnt signaling in vetebrate limb and skeletal developmentZIAHG000187 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI YANG, YINGZI · 2009 to 2015
$7.1M
Wnt signaling in vetebrate limb and skeletal developmentZ01HG000187 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI YANG, YINGZI · 2001 to 2008
$2.9M
Intramural NIH HHS
6 · The paper itself

Abstract

Chondrocyte fate determination and maintenance requires Sox9, an intrinsic transcription factor, but is inhibited by Wnt/beta-catenin signaling activated by extrinsic Wnt ligands. Here we explored the underlying molecular mechanism by which Sox9 antagonizes the Wnt/beta-catenin signaling in chondrocyte differentiation. We found that Sox9 employed two distinct mechanisms to inhibit Wnt/beta-catenin signaling: the Sox9 N terminus is necessary and sufficient to promote beta-catenin degradation, whereas the C terminus is required to inhibit beta-catenin transcriptional activity without affecting its stability. Sox9 binds to beta-catenin and components of the beta-catenin "destruction complex," glycogen synthase kinase 3 and beta-transducin repeat containing protein, to promote their nuclear localization. Independent of its DNA binding ability, nuclear localization of Sox9 is both necessary and sufficient to enhance beta-catenin phosphorylation and its subsequent degradation. Thus, one mechanism whereby Sox9 regulates chondrogenesis is to promote efficient beta-catenin phosphorylation in the nucleus. This mechanism may be broadly employed by other intrinsic cell fate determining transcription factors to promptly turn off extrinsic inhibitory Wnt signaling mediated by beta-catenin.

Indexed as

AnimalsBase Sequencebeta CateninBlotting, WesternCell LineCell NucleusDNA PrimersFluorescent Antibody Technique, IndirectGlycogen Synthase Kinase 3HumansImmunoprecipitationMicePhosphorylationProtein TransportSignal TransductionSOX9 Transcription Factorbeta CateninDNA PrimersGlycogen Synthase Kinase 3Sox9 protein, mouseSOX9 Transcription FactorTransducinWnt Proteins

Identifiers

PMID19047045
PMCPMC2631972
OpenAlexW2140034839

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.