Evidence map›Paper›PMID 9653173›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Autoregulation of thyroid-specific gene transcription by thyroglobulin.

K Suzuki, S Lavaroni, A Mori, M Ohta, J Saito, M Pietrarelli, D S Singer, S Kimura, R Katoh, A Kawaoi and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.

  1. Pooled it
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  10. Review
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  15. Review
  16. Intrinsic regulation of thyroid function by thyroglobulin.Thyroid : official journal of the American Thyroid Association · 2014
    Review
  17. Article
  18. Article
  19. Article
  20. Regulation of dual oxidase expression and H2O2 production by thyroglobulin.Thyroid : official journal of the American Thyroid Association · 2012
    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

11 authors at 3 institutions in 1 country.

K SuzukiMetabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
S Lavaroni
A Mori
M Ohta
J Saito
M Pietrarelli
D S Singer
S Kimura
R Katoh
A Kawaoi
L D Kohn
National Cancer Institute · USNational Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thyroglobulin (TG), the primary synthetic product of the thyroid, is the macromolecular precursor of thyroid hormones. TG synthesis, iodination, storage in follicles, and degradation control thyroid hormone formation and secretion into the circulation. Thyrotropin (TSH), via its receptor (TSHR), increases thyroid hormone levels by up-regulating expression of the sodium iodide symporter (NIS), thyroid peroxidase (TPO), and TG genes. TSH does this by modulating the expression and activity of several thyroid-specific transcription factors, thyroid transcription factor (TTF)-1, TTF-2, and Pax-8, which coordinately regulate NIS, TPO, TG, and the TSHR. Major histocompatibility complex class I gene expression, which also is regulated by TTF-1 and Pax-8 in the thyroid, is decreased simultaneously. This helps maintain self-tolerance in the face of TSH-increased gene products necessary for thyroid hormone formation. In this report we show that follicular TG counter-regulates TSH-increased, thyroid-specific gene transcription by suppressing expression of the TTF-1, TTF-2, and Pax-8 genes. This decreases expression of the TG, TPO, NIS, and TSHR genes, but increases class I expression. TG acts transcriptionally, targeting, for example, a sequence within 1.15 kb of the 5' flanking region of TTF-1. TG does not affect ubiquitous transcription factors regulating TG, TPO, NIS, and/or TSHR gene expression. The inhibitory effect of TG on gene expression is not duplicated by thyroid hormones or iodide and may be mediated by a TG-binding protein on the apical membrane. We hypothesize that TG-initiated, transcriptional regulation of thyroid-restricted genes is a normal, feedback, compensatory mechanism that limits follicular function and contributes to follicular heterogeneity.

Indexed as

Gene Expression RegulationTranscription, GeneticAnimalsAutocrine CommunicationCells, CulturedDNA-Binding ProteinsForkhead Transcription FactorsHistocompatibility Antigens Class INuclear ProteinsPaired Box Transcription FactorsPAX8 Transcription FactorRatsRepressor ProteinsThyroglobulinThyroid GlandThyroid HormonesDNA-Binding ProteinsForkhead Transcription FactorsFOXE1 protein, humanHistocompatibility Antigens Class INKX2-1 protein, humanNkx2-1 protein, ratNuclear ProteinsPaired Box Transcription FactorsPax8 protein, ratPAX8 Transcription FactorRepressor ProteinsThyroglobulinThyroid HormonesThyroid Nuclear Factor 1Trans-ActivatorsTranscription Factors

Identifiers

PMID9653173
PMCPMC20962
OpenAlexW2039205571

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.