Evidence map›Paper›PMID 18474620›Full record

ArticleMolecular and cellular biology2008

Regulation of beta-catenin by a novel nongenomic action of thyroid hormone beta receptor.

Celine J Guigon, Li Zhao, Changxue Lu, Mark C Willingham, Sheue-Yann Cheng

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Thyrotropin, Hyperthyroidism, and Bone Mass.The Journal of clinical endocrinology and metabolism · 2021
    Review
  6. Deiodinases and Cancer.Endocrinology · 2021
    Review
  7. Article
  8. Review
  9. Review
  10. Coding Molecular Determinants of Thyroid Cancer Development and Progression.Endocrinology and metabolism clinics of North America · 2019
    Review
  11. Review
  12. Review
  13. Review
  14. Analysis of Thyroid Tumorigenesis in Xenograft Mouse Model.Methods in molecular biology (Clifton, N.J.) · 2018
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Genetics and epigenetics of sporadic thyroid cancer.Molecular and cellular endocrinology · 2014
    Review
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 4 institutions in 1 country.

Celine J GuigonLaboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-4264, USA.
Li Zhao
Changxue Lu
Mark C Willingham
Sheue-Yann Cheng
Center for Cancer Research · USNational Cancer Institute · USNational Institutes of Health · USWake Forest University · US

Funding

Thyroid Hormone Receptors in Health and DiseaseZIABC008752 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CHENG, SHEUE-YANN · 2009 to 2025
$12.9M
Thyroid Hormone Receptors in Health and DiseaseZ01BC008752 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CHENG, SHEUE-YANN · 1996 to 2008
$2.5M
Intramural NIH HHS
6 · The paper itself

Abstract

We previously created a knock-in mutant mouse harboring a dominantly negative mutant thyroid hormone receptor beta (TRbeta(PV/PV) mouse) that spontaneously develops a follicular thyroid carcinoma similar to human thyroid cancer. We found that beta-catenin, which plays a critical role in oncogenesis, was highly elevated in thyroid tumors of TRbeta(PV/PV) mice. We sought to understand the molecular basis underlying aberrant accumulation of beta-catenin by mutations of TRbeta in vivo. Cell-based studies showed that thyroid hormone (T3) induced the degradation of beta-catenin in cells expressing TRbeta via proteasomal pathways. In contrast, no T3-induced degradation occurred in cells expressing the mutant receptor (TRbetaPV). In vitro binding studies and cell-based analyses revealed that beta-catenin physically associated with unliganded TRbeta or TRbetaPV. However, in the presence of T3, beta-catenin was dissociated from TRbeta-beta-catenin complexes but not from TRbetaPV-beta-catenin complexes. beta-Catenin signaling was repressed by T3 in TRbeta-expressing cells through decreasing beta-catenin-mediated transcription activity and target gene expression, whereas sustained beta-catenin signaling was observed in TRbetaPV-expressing cells. The stabilization of beta-catenin, via association with a mutated TRbeta, represents a novel activating mechanism of the oncogenic protein beta-catenin that could contribute to thyroid carcinogenesis in TRbeta(PV/PV) mice.

Indexed as

Adenomatous Polyposis ColiAnimalsbeta CateninCarcinomaGlycogen Synthase Kinase 3HeLa CellsHumansLigandsMetabolic Networks and PathwaysMiceNuclear ProteinsProteasome Endopeptidase ComplexSeven in Absentia ProteinsSignal TransductionThyroid GlandThyroid Hormone Receptors betabeta CateninGlycogen Synthase Kinase 3LigandsNuclear ProteinsProteasome Endopeptidase ComplexSeven in Absentia ProteinsThyroid Hormone Receptors betaUbiquitin-Protein Ligases

Identifiers

PMID18474620
PMCPMC2447128
OpenAlexW1872414351

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.