Evidence map›Paper›PMID 22878400›Full record

ArticleEndocrinology2012

The thyroid axis is regulated by NCoR1 via its actions in the pituitary.

Ricardo H Costa-e-Sousa, Inna Astapova, Felix Ye, Fredric E Wondisford, Anthony N Hollenberg

Abstract read
In one paragraph

Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. The actions of thyroid hormone signaling in the nucleus.Molecular and cellular endocrinology · 2017
    Review
  11. Congenital hypothyroidism: insights into pathogenesis and treatment.International journal of pediatric endocrinology · 2017
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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

5 authors.

Ricardo H Costa-e-SousaDivision of Endocrinology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.
Inna Astapova
Felix Ye
Fredric E Wondisford
Anthony N Hollenberg

Funding

JHU-UMD Diabetes Research CenterP30DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI AHIMA, REXFORD S. · 2013 to 2017
$9.7M
Diabetes Research and Training CenterP60DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI WONDISFORD, FREDRIC E. · 2008 to 2012
$9.1M
COREPRESSOR REGULATION OF THYROID HORMONE ACTIONR01DK056123 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI HOLLENBERG, ANTHONY N · 2000 to 2023
$7.6M
THYROID HORMONE ACTION IN THE PITUITARYR01DK049126 · NIDDK · UNIVERSITY OF CHICAGO · PI WONDISFORD, FREDRIC E. · 1995 to 2016
$3.8M
Negative regulation by thyroid hormoneR01DK078090 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI HOLLENBERG, ANTHONY N · 2007 to 2010
$1.4M
Corepressor Regulation of Nuclear Receptor ActionR56DK056123 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI HOLLENBERG, ANTHONY N · 2009 to 2009
$425k
NIDDK NIH HHS DK056123NIDDK NIH HHS DK078090NIDDK NIH HHS P30 DK079637NIDDK NIH HHS P60 DK079637NIDDK NIH HHS R01 DK049126NIDDK NIH HHS R01 DK056123NIDDK NIH HHS R01 DK078090NIDDK NIH HHS R01DK49126NIDDK NIH HHS R56 DK056123
6 · The paper itself

Abstract

TSH is the most important biomarker in the interpretation of thyroid function in man. Its levels are determined by circulating thyroid hormone (TH) levels that feed back centrally to regulate the expression of the subunits that comprise TSH from the pituitary. The nuclear corepressor 1 (NCoR1), is a critical coregulator of the TH receptor (TR) isoforms. It has been established to play a major role in the control of TSH secretion, because mice that express a mutant NCoR1 allele (NCoRΔID) that cannot interact with the TR have normal TSH levels despite low circulating TH levels. To determine how NCoR1 controls TSH secretion, we first developed a mouse model that allowed for induction of NCoRΔID expression postnatally to rule out a developmental effect of NCoR1. Expression of NCoRΔID postnatally led to a drop in TH levels without a compensatory rise in TSH production, indicating that NCoR1 acutely controls both TH production and feedback regulation of TSH. To demonstrate that this was a cell autonomous function of NCoR1, we expressed NCoRΔID in the pituitary using a Cre driven by the glycoprotein α-subunit promoter (P-ΔID mice). Importantly, P-ΔID mice have low TH levels with decreased TSH production. Additionally, the rise in TSH during hypothyroidism is blunted in P-ΔID mice. Thus, NCoR1 plays a critical role in TH-mediated regulation of TSH in the pituitary by regulating the repressive function of the TR. Furthermore, these studies suggest that endogenous NCoR1 levels in the pituitary could establish the set point of TSH secretion.

Indexed as

AnimalsFemaleMaleMiceMice, KnockoutNuclear Receptor Co-Repressor 1Pituitary GlandPromoter Regions, GeneticReceptors, Thyroid HormoneThyroid GlandThyrotropinThyrotropin-Releasing HormoneNcor1 protein, mouseNuclear Receptor Co-Repressor 1Receptors, Thyroid HormoneThyrotropinThyrotropin-Releasing Hormone

Identifiers

PMID22878400
PMCPMC3512014

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.