Evidence map›Paper›PMID 20956942›Full record

ArticleOncogene2011

Thyroid hormone receptor β1 domains responsible for the antagonism with the ras oncogene: role of corepressors.

S García-Silva, O Martínez-Iglesias, L Ruiz-Llorente, A Aranda

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Thyroid hormones inhibit TGF-β signaling and attenuate fibrotic responses.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  12. Autoregulatory loop of nuclear corepressor 1 expression controls invasion, tumor growth, and metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  13. Article
  14. Article
  15. Thyroid hormone actions in liver cancer.Cellular and molecular life sciences : CMLS · 2013
    Review
  16. Article
  17. Modeling follicular thyroid cancer for future therapies.American journal of cancer research · 2012
    Article
  18. Article
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

4 authors at 2 institutions in 1 country.

S García-SilvaDepartment of Endocrine and Nervous System Physiopathology, Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid, Madrid, Spain.
O Martínez-Iglesias
L Ruiz-Llorente
A Aranda
Consejo Superior de Investigaciones Científicas · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The thyroid hormone receptor (TR) is a suppressor of ras-mediated responses. To characterize the receptor domains involved in this function, we analyzed a panel of TRβ1 mutants for their ability to interfere with ras-driven cyclin D1 activation, formation of transformation foci and tumor growth in nude mice. Our results show that the domains and mechanisms responsible for the anti-transforming and anti-tumorigenic actions of the receptor are divergent from those operating in classical T3-dependent transcriptional activation. TRβ1 mutants that do not bind coactivators and do not transactivate retained the capacity of suppressing cellular transformation and tumor growth, whereas selective mutations in the hinge region affecting corepressors recruitment abolished these actions, while preserving ligand-dependent transcription. There was a strict parallelism between anti-transforming activity of the various mutants and their ability to antagonize cyclin D1 stimulation by ras, indicating that transrepression mechanisms may have an important function in suppression of the transforming effects of the oncogene by TRβ1. The inhibitory action of T3 on transformation was further enhanced after over-expression of corepressors, while corepressor depletion by means of small-interference RNA reversed significantly hormonal action. This shows an important functional role of endogenous corepressors in suppression of ras-mediated transformation and tumorigenesis by TRβ1.

Indexed as

Genes, rasProtein Interaction Domains and MotifsAnimalsCell Transformation, NeoplasticCo-Repressor ProteinsCyclin D1Hep G2 CellsHumansMiceMice, NudeMutationRNA, Small InterferingThyroid Hormone Receptors betaTriiodothyronineCo-Repressor ProteinsCyclin D1RNA, Small InterferingThyroid Hormone Receptors betaTriiodothyronine

Identifiers

PMID20956942
OpenAlexW2046502116

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.