Evidence map›Paper›PMID 28923959›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

NCoR1-independent mechanism plays a role in the action of the unliganded thyroid hormone receptor.

Arturo Mendoza, Inna Astapova, Hiroaki Shimizu, Molly R Gallop, Lujain Al-Sowaimel, S M Dileas MacGowan, Tim Bergmann, Anders H Berg, Danielle E Tenen, Christopher Jacobs and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-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

20 citing papers in PubMed, 23 citations in OpenAlex.

  1. The abnormal thyroxine signals triggers podocyte apoptosis in DN mice.In vitro cellular & developmental biology. Animal · 2026
    Article
  2. Review
  3. Review
  4. Thyroid Hormone Action by Genomic and Nongenomic Molecular Mechanisms.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  5. Article
  6. Thyroid Hormones and Co-workers: An Overview.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Regulation of Thyroid Hormone Levels by Hypothalamic Thyrotropin-Releasing Hormone Neurons.Thyroid : official journal of the American Thyroid Association · 2023
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

13 authors at 1 institution in 1 country.

Arturo MendozaDivision of Endocrinology Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Boston, MA 02115.ORCID 0000-0002-5142-9718
Inna AstapovaDivision of Endocrinology Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Boston, MA 02115.
Hiroaki ShimizuDivision of Endocrinology Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Boston, MA 02115.
Molly R GallopDivision of Endocrinology Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Boston, MA 02115.
Lujain Al-SowaimelDivision of Endocrinology Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Boston, MA 02115.
S M Dileas MacGowanDivision of Endocrinology Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Boston, MA 02115.
Tim BergmannHarvard Medical School, Boston, MA 02115.
Anders H BergHarvard Medical School, Boston, MA 02115.
Danielle E TenenDivision of Endocrinology Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Boston, MA 02115.
Christopher JacobsDivision of Endocrinology Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Boston, MA 02115.
Anna LyubetskayaDivision of Endocrinology Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Boston, MA 02115.
Linus TsaiDivision of Endocrinology Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Boston, MA 02115.
Anthony N HollenbergDivision of Endocrinology Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Boston, MA 02115; thollenb@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · US

Funding

Transgenic CoreP30DK046200 · NIDDK · TUFTS MEDICAL CENTER · PI GREENBERG, ANDREW S, PERISSI, VALENTINA · 1992 to 2021
$25.0M
COREPRESSOR REGULATION OF THYROID HORMONE ACTIONR01DK056123 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI HOLLENBERG, ANTHONY N · 2000 to 2023
$7.6M
New Targets of Thyroid Hormone ActionR01DK098525 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI HOLLENBERG, ANTHONY N · 2013 to 2017
$2.6M
Corepressor Regulation of Nuclear Receptor ActionR56DK056123 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI HOLLENBERG, ANTHONY N · 2009 to 2009
$425k
NIDDK NIH HHS P30 DK046200NIDDK NIH HHS R01 DK056123NIDDK NIH HHS R01 DK098525NIDDK NIH HHS R56 DK056123
6 · The paper itself

Abstract

Nuclear receptor corepressor 1 (NCoR1) is considered to be the major corepressor that mediates ligand-independent actions of the thyroid hormone receptor (TR) during development and in hypothyroidism. We tested this by expressing a hypomorphic NCoR1 allele (NCoR1ΔID), which cannot interact with the TR, in Pax8-KO mice, which make no thyroid hormone. Surprisingly, abrogation of NCoR1 function did not reverse the ligand-independent action of the TR on many gene targets and did not fully rescue the high mortality rate due to congenital hypothyroidism in these mice. To further examine NCoR1's role in repression by the unliganded TR, we deleted NCoR1 in the livers of euthyroid and hypothyroid mice and examined the effects on gene expression and enhancer activity measured by histone 3 lysine 27 (H3K27) acetylation. Even in the absence of NCoR1 function, we observed strong repression of more than 43% of positive T3 (3,3',5-triiodothyronine) targets in hypothyroid mice. Regulation of approximately half of those genes correlated with decreased H3K27 acetylation, and nearly 80% of these regions with affected H3K27 acetylation contained a bona fide TRβ1-binding site. Moreover, using liver-specific TRβ1-KO mice, we demonstrate that hypothyroidism-associated changes in gene expression and histone acetylation require TRβ1. Thus, many of the genomic changes mediated by the TR in hypothyroidism are independent of NCoR1, suggesting a role for additional signaling modulators in hypothyroidism.

Indexed as

MutationAcetylationAnimalsCells, CulturedGene Expression RegulationHistonesHypothyroidismLiverMiceMice, KnockoutNuclear Receptor Co-Repressor 1Promoter Regions, GeneticSignal TransductionThyroid Hormone Receptors betaThyroid HormonesHistonesNcor1 protein, mouseNuclear Receptor Co-Repressor 1Thyroid Hormone Receptors betaThyroid Hormonesgene repressionhistone acetylationhypothyroidismnegative regulationTRβ1

Identifiers

PMID28923959
PMCPMC5635887
OpenAlexW2755812401

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.