ArticleMolecular and cellular biology2008
Kruppel-like zinc finger protein Glis2 is essential for the maintenance of normal renal functions.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 71 citations in OpenAlex.
- SARS-CoV-2 nonspike structural proteins hijack mucosa epithelial cell fate.Cell death & disease · 2026Article
- PRDM16 acts as a homeostasis regulation factor to suppress the transition of AKI to CKD via upregulation of eukaryotic initiation factor 6.Cellular and molecular life sciences : CMLS · 2025Article
- Transcription factor roles in the local adaptation to temperature in the Andean Spiny Toad Rhinella spinulosa.Scientific reports · 2024Article
- Glis2 is an early effector of polycystin signaling and a target for therapy in polycystic kidney disease.Nature communications · 2024Article
- Identifying cellular senescence associated genes involved in the progression of end-stage renal disease as new biomarkers.BMC nephrology · 2023Article
- Transcriptional regulation of Glis2 in hepatic fibrosis.Experimental & molecular medicine · 2023Article
- Microvascular and macrovascular complications of type 2 diabetes mellitus: Exome wide association analyses.Frontiers in endocrinology · 2023Article
- Review
- p75Neurotoxicity research · 2022Article
- Loureirin B Alleviates Myocardial Ischemia/Reperfusion Injury via Inhibiting PAI-1/TGF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
- An EMT-primary cilium-GLIS2 signaling axis regulates mammogenesis and claudin-low breast tumorigenesis.Science advances · 2021Article
- Distinct Murine Pancreatic Transcriptomic Signatures during Chronic Pancreatitis Recovery.Mediators of inflammation · 2021Article
- Renal Ciliopathies: Sorting Out Therapeutic Approaches for Nephronophthisis.Frontiers in cell and developmental biology · 2021Review
- Transcription factor GLIS3: Critical roles in thyroid hormone biosynthesis, hypothyroidism, pancreatic beta cells and diabetes.Pharmacology & therapeutics · 2020Review
- Innate Immune Signaling Contributes to Tubular Cell Senescence in the Glis2 Knockout Mouse Model of Nephronophthisis.The American journal of pathology · 2020Article
- 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
- Prominin-1 controls stem cell activation by orchestrating ciliary dynamics.The EMBO journal · 2019Article
- Low Expression of GLIS2 Gene Might Associate with Radiosensitivity of Gastric Cancer.Journal of oncology · 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
7 authors at 3 institutions in 1 country.
Funding
Abstract
To obtain insight into the physiological functions of the Krüppel-like zinc finger protein Gli-similar 2 (Glis2), mice deficient in Glis2 expression were generated. Glis2 mutant (Glis2(mut)) mice exhibit significantly shorter life spans than do littermate wild-type (WT) mice due to the development of progressive chronic kidney disease with features resembling nephronophthisis. Glis2(mut) mice develop severe renal atrophy involving increased cell death and basement membrane thickening in the proximal convoluted tubules. This development is accompanied by infiltration of lymphocytic inflammatory cells and interstitial/glomerular fibrosis. The severity of the fibrosis, inflammatory infiltrates, and glomerular and tubular changes progresses with age. Blood urea nitrogen and creatinine increase, and Glis2(mut) mice develop proteinuria and ultimately die prematurely of renal failure. A comparison of the gene expression profiles of kidneys from 25-day-old/60-day-old WT and Glis2(mut) mice by microarray analysis showed increased expressions of many genes involved in immune responses/inflammation and fibrosis/tissue remodeling in kidneys of Glis2(mut) mice, including several cytokines and adhesion and extracellular matrix proteins. Our data demonstrate that a deficiency in Glis2 expression leads to tubular atrophy and progressive fibrosis, similar to nephronophthisis, that ultimately results in renal failure. Our study indicates that Glis2 plays a critical role in the maintenance of normal kidney architecture and functions.
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