Evidence map›Paper›PMID 32245491›Full record

ReviewCell communication and signaling : CCS2020

GLI3: a mediator of genetic diseases, development and cancer.

Stephan J Matissek, Sherine F Elsawa

Open access · goldAbstract readReviewVideo-Audio Media
In one paragraph

Review in Cell communication and signaling : CCS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

87 citing papers in PubMed, 132 citations in OpenAlex.

  1. Trial
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  7. [Molecular cancer · 2026
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  12. NovelPathology oncology research : POR · 2026
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27 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Stephan J MatissekDepartment of Molecular, Cellular and Biomedical Sciences, University of New Hampshire, 46 College Rd Rudman 291, Durham, NH, 03824, USA.
Sherine F ElsawaDepartment of Molecular, Cellular and Biomedical Sciences, University of New Hampshire, 46 College Rd Rudman 291, Durham, NH, 03824, USA. sherine.elsawa@unh.edu.
University of New Hampshire · US

Funding

TLR-TRIF mediated induction of GLI3 modulates innate inflammatory responsesP20GM113131 · NIGMS · UNIVERSITY OF NEW HAMPSHIRE · PI Sean Stoddart Coleman Edington · 2017 to 2026
$22.8M
NIGMS NIH HHS P20 GM113131
6 · The paper itself

Abstract

The transcription factor GLI3 is a member of the Hedgehog (Hh/HH) signaling pathway that can exist as a full length (Gli3-FL/GLI3-FL) or repressor (Gli3-R/GLI3-R) form. In response to HH activation, GLI3-FL regulates HH genes by targeting the GLI1 promoter. In the absence of HH signaling, GLI3 is phosphorylated leading to its partial degradation and the generation of GLI3-R which represses HH functions. GLI3 is also involved in tissue development, immune cell development and cancer. The absence of Gli3 in mice impaired brain and lung development and GLI3 mutations in humans are the cause of Greig cephalopolysyndactyly (GCPS) and Pallister Hall syndromes (PHS). In the immune system GLI3 regulates B, T and NK-cells and may be involved in LPS-TLR4 signaling. In addition, GLI3 was found to be upregulated in multiple cancers and was found to positively regulate cancerous behavior such as anchorage-independent growth, angiogenesis, proliferation and migration with the exception in acute myeloid leukemia (AML) and medulloblastoma where GLI plays an anti-cancerous role. Finally, GLI3 is a target of microRNA. Here, we will review the biological significance of GLI3 and discuss gaps in our understanding of this molecule. Video Abstract.

Indexed as

NeoplasmsNerve Tissue ProteinsOrganogenesisZinc Finger Protein Gli3AnimalsGenetic Diseases, InbornHumansImmune SystemMiceGLI3 protein, humanGli3 protein, mouseNerve Tissue ProteinsZinc Finger Protein Gli3CancerDevelopmentGenetic diseaseGLIGLI3Hedgehog signaling

Identifiers

PMID32245491
PMCPMC7119169
OpenAlexW3015140931

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.