ReviewHistology and histopathology2010
Gli-similar (Glis) Krüppel-like zinc finger proteins: insights into their physiological functions and critical roles in neonatal diabetes and cystic renal disease.
Review in Histology and histopathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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.
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.
Who cites it
45 citing papers in PubMed, 54 citations in OpenAlex.
- A Novel Renal Manifestation inJournal of medical cases · 2026Article
- [Acute megakaryoblastic leukemia with CBFA2T3::GLIS2 fusion gene: 3 cases report and literature review].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Review
- Glis3 as a critical regulator of Pit1-lineages and renal functions.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Tri-domain proteins 27 alleviates ischemia-reperfusion injury-induced acute kidney injury by promoting Gli-like transcription factor 1 expression via the inhibition of polycomb repressive complex 2 activity.Journal of cell communication and signaling · 2025Article
- Distinct Roles of Common Genetic Variants and Their Contributions to Diabetes: MODY and Uncontrolled T2DM.Biomolecules · 2025Review
- Glis2 is an early effector of polycystin signaling and a target for therapy in polycystic kidney disease.Nature communications · 2024Article
- The Role of BDNF, YBX1, CENPF, ZSCAN4, TEAD4, GLIS1 and USF1 in the Activation of the Embryonic Genome in Bovine Embryos.International journal of molecular sciences · 2023Review
- Malakoplakia with aberrant ALK expression by immunohistochemistry: a case report.Diagnostic pathology · 2023Article
- Transcriptional regulation of Glis2 in hepatic fibrosis.Experimental & molecular medicine · 2023Article
- GLIS1 intervention enhances anti-PD1 therapy for hepatocellular carcinoma by targeting SGK1-STAT3-PD1 pathway.Journal for immunotherapy of cancer · 2023Article
- The gene regulatory molecule GLIS3 in gastric cancer as a prognostic marker and be involved in the immune infiltration mechanism.Frontiers in oncology · 2023Article
- Review
- Article
- Identification of Optimal Expression Parameters and Purification of a Codon-Optimized Human GLIS1 Transcription Factor from Escherichia coli.Molecular biotechnology · 2022Article
- Cystic Fibrosis-Related Diabetes (CFRD): Overview of Associated Genetic Factors.Diagnostics (Basel, Switzerland) · 2021Review
- 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
- Case Report: Neonatal Diabetes Mellitus Caused by a NovelFrontiers 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
GLI-similar (Glis) 1-3 proteins constitute a subfamily of the Krüppel-like zinc finger transcription factors that are closely related to the Gli family. Glis1-3 play critical roles in the regulation of a number of physiological processes and have been implicated in several pathologies. Mutations in GLIS2 have been linked to nephronophthisis, an autosomal recessive cystic kidney disease. Loss of Glis2 function leads to renal atrophy and fibrosis that involves epithelial-mesenchymal transition (EMT) of renal tubule epithelial cells. Mutations in human GLIS3 have been implicated in a syndrome characterized by neonatal diabetes and congenital hypothyroidism (NDH) and in some patients accompanied by polycystic kidney disease, glaucoma, and liver fibrosis. In addition, the GLIS3 gene has been identified as a susceptibility locus for the risk of type 1 and 2 diabetes. Glis3 plays a key role in pancreatic development, particularly in the generation of ß-cells and in the regulation of insulin gene expression. Glis2 and Glis3 proteins have been demonstrated to localize to the primary cilium, a signaling organelle that has been implicated in several pathologies, including cystic renal diseases. This association suggests that Glis2/3 are part of primary cilium-associated signaling pathways that control the activity of Glis proteins. Upon activation in the primary cilium, Glis proteins may translocate to the nucleus where they subsequently regulate gene transcription by interacting with Glis-binding sites in the promoter regulatory region of target genes. In this review, we discuss the current knowledge of the Glis signaling pathways, their physiological functions, and their involvement in several human pathologies.
Indexed as
Identifiers
What OpenQuestion holds
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.