Evidence map›Paper›PMID 19273592›Full record

ArticleMolecular and cellular biology2009

Glis3 is associated with primary cilia and Wwtr1/TAZ and implicated in polycystic kidney disease.

Hong Soon Kang, Ju Youn Beak, Yong-Sik Kim, Ronald Herbert, Anton M Jetten

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
5.2field-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

65 citing papers in PubMed, 98 citations in OpenAlex.

  1. A Novel Renal Manifestation inJournal of medical cases · 2026
    Article
  2. Glis3 Is a Modifier of Cyst Progression in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026
    Article
  3. Article
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  7. Glis3 as a critical regulator of Pit1-lineages and renal functions.Journal of molecular medicine (Berlin, Germany) · 2025
    Article
  8. Article
  9. Article
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  11. Article
  12. International journal of molecular sciences · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. The role of primary cilia in thyroid diseases.Frontiers in endocrinology · 2023
    Review
  20. Review

5 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

5 authors at 1 institution in 1 country.

Hong Soon KangLRB, Cell Biology Section, Division of Intramural Research, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Ju Youn Beak
Yong-Sik Kim
Ronald Herbert
Anton M Jetten
National Institutes of Health · US

Funding

Mechanism Of Action And Functions Of The Gli-related Proteins Glis 1-3ZIAES100485 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI JETTEN, ANTON M · 2009 to 2025
$35.9M
CMPB Central Pathology SupportZIGES102505 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI SILLS, ROBERT · 2010 to 2013
$35.4M
CMPB Central Pathology SupportZ01ES102505 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI SILLS, ROBERT · 2008 to 2008
$5.7M
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
6 · The paper itself

Abstract

In this study, we describe the generation and partial characterization of Krüppel-like zinc finger protein Glis3 mutant (Glis3(zf/zf)) mice. These mice display abnormalities very similar to those of patients with neonatal diabetes and hypothyroidism syndrome, including the development of diabetes and polycystic kidney disease. We demonstrate that Glis3 localizes to the primary cilium, suggesting that Glis3 is part of a cilium-associated signaling pathway. Although Glis3(zf/zf) mice form normal primary cilia, renal cysts contain relatively fewer cells with a primary cilium. We further show that Glis3 interacts with the transcriptional modulator Wwtr1/TAZ, which itself has been implicated in glomerulocystic kidney disease. Wwtr1 recognizes a P/LPXY motif in the C terminus of Glis3 and enhances Glis3-mediated transcriptional activation, indicating that Wwtr1 functions as a coactivator of Glis3. Mutations in the P/LPXY motif abrogate the interaction with Wwtr1 and the transcriptional activity of Glis3, indicating that this motif is part of the transcription activation domain of Glis3. Our study demonstrates that dysfunction of Glis3 leads to the development of cystic renal disease, suggesting that Glis3 plays a critical role in maintaining normal renal functions. We propose that localization to the primary cilium and interaction with Wwtr1 are key elements of the Glis3 signaling pathway.

Indexed as

14-3-3 ProteinsAbnormalities, MultipleAdaptor Proteins, Signal TransducingAnimalsCell AdhesionCiliaDNA-Binding ProteinsGene Expression RegulationHumansKidneyKruppel-Like Transcription FactorsMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsPolycystic Kidney Diseases14-3-3 ProteinsAdaptor Proteins, Signal TransducingDNA-Binding ProteinsGli5 protein, mouseGlis3 protein, mouseKruppel-Like Transcription FactorsNerve Tissue ProteinsRepressor ProteinsTrans-ActivatorsWwtr1 protein, mouse

Identifiers

PMID19273592
PMCPMC2682055
OpenAlexW2102053088

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.