Evidence map›Paper›PMID 22570333›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2012

Fundamentally distinct roles of thyroid hormone receptor isoforms in a thyrotroph cell line are due to differential DNA binding.

Maria I Chiamolera, Aniket R Sidhaye, Shunichi Matsumoto, Qiyi He, Koshi Hashimoto, Tania M Ortiga-Carvalho, Fredric E Wondisford

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Expression and Regulation ofFrontiers in physiology · 2020
    Article
  9. Review
  10. Article
  11. The actions of thyroid hormone signaling in the nucleus.Molecular and cellular endocrinology · 2017
    Review
  12. Article
  13. New insights into thyroid hormone action.Pharmacology & therapeutics · 2017
    Review
  14. Advances in TRH signaling.Reviews in endocrine & metabolic disorders · 2016
    Review
  15. A review of the peripheral levels of regulation by thyroid hormone.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2016
    Review
  16. Tissue thyroid hormones and thyronamines.Heart failure reviews · 2016
    Review
  17. Article
  18. Review
  19. Article
  20. 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

7 authors at 5 institutions in 3 countries.

Maria I ChiamoleraUniversidade Federal de Sao Paulo, 05508-900 Sao Paulo, Brazil.
Aniket R Sidhaye
Shunichi Matsumoto
Qiyi He
Koshi Hashimoto
Tania M Ortiga-Carvalho
Fredric E Wondisford
Johns Hopkins University · USGunma University · JPJohns Hopkins Medicine · USUniversidade Federal de São Paulo · BRUniversidade Federal do Rio de Janeiro · BR

Funding

JHU-UMD Diabetes Research CenterP30DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI AHIMA, REXFORD S. · 2013 to 2017
$9.7M
THYROID HORMONE ACTION IN THE PITUITARYR01DK049126 · NIDDK · UNIVERSITY OF CHICAGO · PI WONDISFORD, FREDRIC E. · 1995 to 2016
$3.8M
NIDDK NIH HHS P30 DK079637NIDDK NIH HHS P60DK07963NIDDK NIH HHS R01 DK049126NIDDK NIH HHS R01DK049126
6 · The paper itself

Abstract

Thyroid hormones have a profound influence on human development and disease. The hypothalamic-pituitary-thyroid axis involves finely tuned feedback mechanisms to maintain thyroid hormone (TH) levels. Despite the important role of TH-negative feedback in regulating this axis, the mechanism by which this occurs is not clearly defined. Previous in vivo studies suggest separate roles for the two thyroid hormone receptor isoforms, THRA and THRB, in this axis. We performed studies using a unique pituitary thyrotroph cell line (TαT1.1) to determine the relative roles of THRA and THRB in the regulation of Tshb. Using chromatin immunoprecipitation assays, we found that THRB, not THRA, bound to the Tshb promoter. By selectively depleting THRB, THRA, or both THRA and THRB in TαT1.1 cells, we found that simultaneous knockdown of both THRB and THRA abolished T(3)-mediated down-regulation of Tshb at concentrations as high as 100 nm T(3). In contrast, THRA knockdown alone had no effect on T(3)-negative regulation, whereas THRB knockdown alone abolished T(3)-mediated down-regulation of Tshb mRNA levels at 10 nm but not 100 nm T(3) concentrations. Interestingly, chromatin immunoprecipitation assays showed that THRA becomes enriched on the Tshb promoter after knockdown of THRB. Thus, a likely mechanism for the differential effects of THR isoforms on Tshb may be based on their differential DNA-binding affinity to the promoter.

Indexed as

AnimalsCell LineDNAGene Expression RegulationGene Knockdown TechniquesGlycoprotein Hormones, alpha SubunitMicePromoter Regions, GeneticProtein BindingProtein IsoformsReceptors, Thyroid HormoneRNA InterferenceRNA, MessengerThyrotrophsThyrotropin, beta SubunitTranscription, GeneticDNAGlycoprotein Hormones, alpha SubunitProtein IsoformsReceptors, Thyroid HormoneRNA, MessengerThyrotropin, beta SubunitTriiodothyronine

Identifiers

PMID22570333
PMCPMC3355539
OpenAlexW2000570774

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.