Evidence map›Paper›PMID 32693112›Full record

ReviewPharmacology & therapeutics2020

Transcription factor GLIS3: Critical roles in thyroid hormone biosynthesis, hypothyroidism, pancreatic beta cells and diabetes.

David W Scoville, Hong Soon Kang, Anton M Jetten

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.7field-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

28 citing papers in PubMed, 48 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

David W ScovilleCell Biology Group, Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Hong Soon KangCell Biology Group, Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Anton M JettenCell Biology Group, Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: jetten@niehs.nih.gov.
National Institute of Environmental Health Sciences · USNational Institutes of Health · US

Funding

Mechanism Of Action And Functions Of The Gli-related Proteins Glis 1-3Z01ES100485 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI JETTEN, ANTON M · 2002 to 2008
$2.3M
Intramural NIH HHS Z01 ES100485
6 · The paper itself

Abstract

GLI-Similar 3 (GLIS3) is a member of the GLIS subfamily of Krüppel-like zinc finger transcription factors that functions as an activator or repressor of gene expression. Study of GLIS3-deficiency in mice and humans revealed that GLIS3 plays a critical role in the regulation of several biological processes and is implicated in the development of various diseases, including hypothyroidism and diabetes. This was supported by genome-wide association studies that identified significant associations of common variants in GLIS3 with increased risk of these pathologies. To obtain insights into the causal mechanisms underlying these diseases, it is imperative to understand the mechanisms by which this protein regulates the development of these pathologies. Recent studies of genes regulated by GLIS3 led to the identification of a number of target genes and have provided important molecular insights by which GLIS3 controls cellular processes. These studies revealed that GLIS3 is essential for thyroid hormone biosynthesis and identified a critical function for GLIS3 in the generation of pancreatic β cells and insulin gene transcription. These observations raised the possibility that the GLIS3 signaling pathway might provide a potential therapeutic target in the management of diabetes, hypothyroidism, and other diseases. To develop such strategies, it will be critical to understand the upstream signaling pathways that regulate the activity, expression and function of GLIS3. Here, we review the recent progress on the molecular mechanisms by which GLIS3 controls key functions in thyroid follicular and pancreatic β cells and how this causally relates to the development of hypothyroidism and diabetes.

Indexed as

AnimalsDiabetes MellitusDNA-Binding ProteinsGenome-Wide Association StudyHumansHypothyroidismInsulinInsulin-Secreting CellsMiceRepressor ProteinsThyroid HormonesTrans-ActivatorsDNA-Binding ProteinsGLIS3 protein, humanInsulinRepressor ProteinsThyroid HormonesTrans-ActivatorsDiabetesGene transcriptionHypothyroidismInsulinPancreatic β cellsThyroid hormone biosynthesis

Identifiers

PMID32693112
PMCPMC7606550
OpenAlexW3043425595

What OpenQuestion holds

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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.