ArticleOncogene2004
Unliganded thyroid hormone receptor beta1 inhibits proliferation of murine fibroblasts by delaying the onset of the G1 cell-cycle signals.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
The trial behind it
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- DIO3 coordinates photoreceptor development timing and fate stability in human retinal organoids.Genes & development · 2026Article
- Thyroid Hormone Receptor Beta as Tumor Suppressor: Untapped Potential in Treatment and Diagnostics in Solid Tumors.Cancers · 2021Review
- Implication from thyroid function decreasing during chemotherapy in breast cancer patients: chemosensitization role of triiodothyronine.BMC cancer · 2013Article
- Cellular and molecular basis of deiodinase-regulated thyroid hormone signaling.Endocrine reviews · 2008Review
- Thyroid hormone - triiodothyronine - has contrary effect on proliferation of human proximal tubules cell line (HK2) and renal cancer cell lines (Caki-2, Caki-1) - role of E2F4, E2F5 and p107, p130.Thyroid research · 2008Article
- Thyroid hormone receptor-beta (TR beta 1) impairs cell proliferation by the transcriptional inhibition of cyclins D1, E and A2.Oncogene · 2008Article
- Sonic hedgehog-induced type 3 deiodinase blocks thyroid hormone action enhancing proliferation of normal and malignant keratinocytes.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid hormone receptors (TRs) are members of the ligand-inducible transcription factor superfamily. The two major functional TRs (alpha1 and beta1) have different spatial and temporal expression patterns and specific physiological functions for these isoforms are now starting to emerge. By expressing these TR isoforms individually in Swiss 3T3 fibroblasts, we found that TRbeta1 expression, in the absence of hormone, provokes a proliferation arrest in G0/G1, lengthening the cycling time. Upon serum stimulation TRbeta1-expressing cells showed a marked delay in the induction of cyclins D and E, in the phosphorylation of retinoblastoma protein, and in the activation of cyclin-dependent kinase 2, accompanied by increased levels of cyclin-dependent kinase inhibitor p27Kip1. Accordingly, serum-stimulated E2F-1 transcriptional activity was repressed by TRbeta1 in transient transfection experiments. Analysis of the receptor domains required for this effect confirmed that there is no need for a functional ligand-binding domain while the DNA-binding domain is essential. In this work, we demonstrate for the first time that TRbeta1 participates in the molecular mechanisms that control cell proliferation. The unliganded TRbeta1 impairs the normal induction of the G1/S cycle regulators preventing progression into the S phase.
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Registered trials
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.