ArticleNucleic acids research2008
Functional analysis of the zinc finger and activation domains of Glis3 and mutant Glis3(NDH1).
Article in Nucleic acids research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Pathogenic monoallelic variants in GLIS3 increase type 2 diabetes risk and identify a subgroup of patients sensitive to sulfonylureas.Diabetologia · 2024Pooled it
- Glis3 Is a Modifier of Cyst Progression in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Article
- GLIS3, a novel regulator of eicosanoid gene expression and metabolism in normal kidney and polycystic kidney disease.Biochemical pharmacology · 2026Article
- Identification of distinct functions of GLIS3 in β-cell generation critical to prevention of neonatal diabetes.bioRxiv : the preprint server for biology · 2026Article
- Alternative Splicing (AS) Provides an Alternative Mechanism for Regulating GLIS3 Expression and Activity.Cells · 2025Article
- Article
- Adaptive introgression reveals the genetic basis of a sexually selected syndrome in wall lizards.Science advances · 2024Article
- The compensatory increase of Gli-similar 3 inhibited neuronal apoptosis through regulating Mps one binder kinase activator 1b (MOB1b): a possible strategy for the functional recovery after spinal cord injury.Experimental animals · 2024Article
- Neonatal Diabetes, Congenital Hypothyroidism, and Congenital Glaucoma Coexistence: A Case ofJournal of clinical research in pediatric endocrinology · 2023Article
- Polycystin-2-dependent transcriptome reveals early response of autosomal dominant polycystic kidney disease.Physiological genomics · 2023Article
- GLIS1 regulates trabecular meshwork function and intraocular pressure and is associated with glaucoma in humans.Nature communications · 2021Article
- Neonatal diabetes mutations disrupt a chromatin pioneering function that activates the human insulin gene.Cell reports · 2021Article
- Association study of the functional variants of the GLIS3 gene with risk of knee osteoarthritis.Clinical rheumatology · 2021Article
- Case Report: Neonatal Diabetes Mellitus Caused by a NovelFrontiers in endocrinology · 2021Article
- Case Report: Extended Clinical Spectrum of the Neonatal Diabetes With Congenital Hypothyroidism Syndrome.Frontiers in endocrinology · 2021Article
- Transcription factor GLIS3: Critical roles in thyroid hormone biosynthesis, hypothyroidism, pancreatic beta cells and diabetes.Pharmacology & therapeutics · 2020Review
- Evolutionary History of GLIS Genes Illuminates Their Roles in Cell Reprograming and Ciliogenesis.Molecular biology and evolution · 2020Article
- Emerging Roles of GLI-Similar Krüppel-like Zinc Finger Transcription Factors in Leukemia and Other Cancers.Trends in cancer · 2019Review
- GLIS3 Transcriptionally Activates WNT Genes to Promote Differentiation of Human Embryonic Stem Cells into Posterior Neural Progenitors.Stem cells (Dayton, Ohio) · 2019Article
- GLIS1-3 transcription factors: critical roles in the regulation of multiple physiological processes and diseases.Cellular and molecular life sciences : CMLS · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The Krüppel-like zinc finger protein Gli-similar 3 (Glis3) plays a critical role in pancreatic development and has been implicated in a syndrome with neonatal diabetes and hypothyroidism (NDH). In this study, we examine three steps critical in the mechanism of the transcriptional regulation by Glis3: its translocation to the nucleus, DNA binding and transcriptional activity. We demonstrate that the putative bipartite nuclear localization signal is not required, but the tetrahedral configuration of the fourth zinc finger is essential for the nuclear localization of Glis3. We identify (G/C)TGGGGGGT(A/C) as the consensus sequence of the optimal, high-affinity Glis3 DNA-binding site (Glis-BS). All five zinc finger motifs are critical for efficient binding of Glis3 to Glis-BS. We show that Glis3 functions as a potent inducer of (Glis-BS)-dependent transcription and contains a transactivation function at its C-terminus. A mutation in Glis3 observed in NDH1 patients results in a frameshift mutation and a C-terminal truncated Glis3. We demonstrate that this truncation does not effect the nuclear localization but results in the loss of Glis3 transactivating activity. The loss in Glis3 transactivating function may be responsible for the abnormalities observed in NDH1.
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Registered trials
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.