ArticleThe Journal of biological chemistry2011
Identification of nuclear localization, DNA binding, and transactivating mechanisms of Kruppel-like zinc finger protein Gli-similar 2 (Glis2).
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- GLIS2 Promotes Epithelial-Mesenchymal Transition and Gastric Cancer Progression by Regulating BGN to Activate the Wnt/β-Catenin Pathway.The Kaohsiung journal of medical sciences · 2026Article
- Glis3 as a critical regulator of Pit1-lineages and renal functions.Journal of molecular medicine (Berlin, Germany) · 2025Article
- CBFA2T3-GLIS2 mediates transcriptional regulation of developmental pathways through a gene regulatory network.Nature communications · 2024Article
- Transcriptional regulation of Glis2 in hepatic fibrosis.Experimental & molecular medicine · 2023Article
- High caspase 3 and vulnerability to dual BCL2 family inhibition define ETO2::GLIS2 pediatric leukemia.Leukemia · 2023Article
- p75Neurotoxicity research · 2022Article
- A direct comparison between AML1-ETO and ETO2-GLIS2 leukemia fusion proteins reveals context-dependent binding and regulation of target genes and opposite functions in cell differentiation.Frontiers in cell and developmental biology · 2022Article
- Hedgehog/GLI Signaling Pathway: Transduction, Regulation, and Implications for Disease.Cancers · 2021Review
- Genetic response to low‑intensity ultrasound on mouse ST2 bone marrow stromal cells.Molecular medicine reports · 2021Article
- GLIS Family Zinc Finger 1 was First Linked With Preaxial Polydactyly I in Humans by Stepwise Genetic Analysis.Frontiers in cell and developmental biology · 2021Article
- 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
- CBFA2T3-GLIS2-positive acute myeloid leukaemia. A peculiar paediatric entity.British journal of haematology · 2019Review
- GLIS1-3 transcription factors: critical roles in the regulation of multiple physiological processes and diseases.Cellular and molecular life sciences : CMLS · 2018Review
- GLIS1-3: emerging roles in reprogramming, stem and progenitor cell differentiation and maintenance.Stem cell investigation · 2017Review
- The C175R mutation alters nuclear localization and transcriptional activity of the nephronophthisis NPHP7 gene product.European journal of human genetics : EJHG · 2016Article
- An in vivo screen to identify candidate neurogenic genes in the developing Xenopus visual system.Developmental biology · 2015Article
- Up-regulation of Glis2 involves in neuronal apoptosis after intracerebral hemorrhage in adult rats.Cellular and molecular neurobiology · 2015Article
- SUMOylation Blocks the Ubiquitin-Mediated Degradation of the Nephronophthisis Gene Product Glis2/NPHP7.PloS one · 2015Article
- Interaction with the Bardet-Biedl gene product TRIM32/BBS11 modifies the half-life and localization of Glis2/NPHP7.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Gli-similar 1-3 (Glis1-3) constitute a subfamily of Krüppel-like zinc finger (ZF) transcription factors that are closely related to the Gli protein family. Mutations in GLIS2 are linked to nephronophthisis, a chronic kidney disease characterized by renal fibrosis and atrophy in children and young adults. Currently, very little information exists about the mechanism of action of Glis2, its target genes, or the signaling pathways that regulate its activity. In this study, we show that a region within ZF3 is required for the nuclear localization of Glis2. Analysis of Glis2 DNA binding demonstrated that Glis2 binds effectively to the consensus Glis binding sequence (GlisBS) (G/C)TGGGGGGT(A/C). Although Glis2 was unable to induce transactivation of a GlisBS-dependent reporter, it effectively inhibited the GlisBS-mediated transactivation by Gli1. Mutations that disrupt the tetrahedral configuration of each ZF within Glis2 abolished Glis2 binding to GlisBS and also abrogated its inhibition of Gli1-mediated transactivation. In contrast, Glis2 was able to activate the murine insulin-2 (Ins2) promoter by binding directly to two GlisBS elements located at -263 and -99 within the Ins2 promoter. Phosphomimetic mutation of Ser(245) inhibited the binding of Glis2 to GlisBS and dramatically affected its transactivation of the Ins2 promoter and its ability to inhibit GlisBS-dependent transactivation by Gli1. In this study, we demonstrate that Glis2 can function as a transcriptional activator and that post-translational modification within its DNA-binding domain can regulate its transcriptional activity. This control may play a critical role in the Glis2-dependent regulation of target genes and renal function.
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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.