Evidence map›Paper›PMID 24558356›Full record

ArticlePloS one2014

Genome-wide binding patterns of thyroid hormone receptor beta.

Stephen Ayers, Michal Piotr Switnicki, Anusha Angajala, Jan Lammel, Anithachristy S Arumanayagam, Paul Webb

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.4field-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

34 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. The TSH/Thyroid Hormones Axis and Breast Cancer.Journal of clinical medicine · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Thyroid hormone receptor β1 stimulatesJournal of lipid research · 2018
    Article
  19. Article
  20. 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

6 authors at 2 institutions in 2 countries.

Stephen AyersThe Methodist Hospital Research Institute, Genomic Medicine Program, Houston, Texas, United States of America.
Michal Piotr SwitnickiThe Methodist Hospital Research Institute, Genomic Medicine Program, Houston, Texas, United States of America.
Anusha AngajalaThe Methodist Hospital Research Institute, Genomic Medicine Program, Houston, Texas, United States of America.
Jan LammelThe Methodist Hospital Research Institute, Genomic Medicine Program, Houston, Texas, United States of America ; Tecnologico de Monterrey School of Medicine, Monterrey, NL, Mexico.
Anithachristy S ArumanayagamThe Methodist Hospital Research Institute, Genomic Medicine Program, Houston, Texas, United States of America.
Paul WebbThe Methodist Hospital Research Institute, Genomic Medicine Program, Houston, Texas, United States of America.
Methodist Hospital · USHouston Methodist · US

Funding

Optimal Selective Thyroid Hormone Analogs for Metabolic SyndromeRC4DK090849 · NIDDK · METHODIST HOSPITAL RESEARCH INSTITUTE · PI WEBB, PAUL · 2010 to 2010
$2.9M
NIDDK NIH HHS RC4 DK090849
6 · The paper itself

Abstract

Thyroid hormone (TH) receptors (TRs) play central roles in metabolism and are major targets for pharmaceutical intervention. Presently, however, there is limited information about genome wide localizations of TR binding sites. Thus, complexities of TR genomic distribution and links between TRβ binding events and gene regulation are not fully appreciated. Here, we employ a BioChIP approach to capture TR genome-wide binding events in a liver cell line (HepG2). Like other NRs, TRβ appears widely distributed throughout the genome. Nevertheless, there is striking enrichment of TRβ binding sites immediately 5' and 3' of transcribed genes and TRβ can be detected near 50% of T3 induced genes. In contrast, no significant enrichment of TRβ is seen at negatively regulated genes or genes that respond to unliganded TRs in this system. Canonical TRE half-sites are present in more than 90% of TRβ peaks and classical TREs are also greatly enriched, but individual TRE organization appears highly variable with diverse half-site orientation and spacing. There is also significant enrichment of binding sites for TR associated transcription factors, including AP-1 and CTCF, near TR peaks. We conclude that T3-dependent gene induction commonly involves proximal TRβ binding events but that far-distant binding events are needed for T3 induction of some genes and that distinct, indirect, mechanisms are often at play in negative regulation and unliganded TR actions. Better understanding of genomic context of TR binding sites will help us determine why TR regulates genes in different ways and determine possibilities for selective modulation of TR action.

Indexed as

Binding SitesAnimalsCell LineGene Expression RegulationGenomeHep G2 CellsHumansLigandsLiverMiceMice, Inbred C57BLMultigene FamilyOligonucleotide Array Sequence AnalysisPlasmidsProtein BindingResponse ElementsLigandsRNAThyroid Hormone Receptors beta

Identifiers

PMID24558356
PMCPMC3928038
OpenAlexW2045256303

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.