ArticleNature communications2024
Glis2 is an early effector of polycystin signaling and a target for therapy in polycystic kidney disease.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 21 citations in OpenAlex.
- Evidence for a tubular basement membrane-cilia connection in autosomal dominant polycystic kidney disease pathogenesis.The Journal of clinical investigation · 2026Article
- Cilia-to-basement membrane signaling is a biomechanical driver in models of autosomal dominant polycystic kidney disease.The Journal of clinical investigation · 2026Article
- Fibrocystin/polyductin (FPC): new functional insights into ARPKD pathogenesis revealed by informatics, comparative genomics, and model systems.Pediatric nephrology (Berlin, Germany) · 2026Review
- Kidney-specific deletion of the BicC family RNA-binding protein 1 triggers an ADPKD-like cystogenic program.iScience · 2026Article
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- Cerebrovascular vulnerability and fibrosis in human brain aneurysms.Nature neuroscience · 2026Article
- Glis3 Is a Modifier of Cyst Progression in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Article
- Collecting Duct-Targeted Lipid Nanoparticles DeliverbioRxiv : the preprint server for biology · 2026Article
- Toward Physiologically Relevant Organoid Models of Polycystic Kidney Disease through Microenvironment Reconstruction.Journal of the American Society of Nephrology : JASN · 2026Review
- Miniaturization of CRISPRa plasmids for efficient delivery into renal epithelial cells and Pkd1 transactivation.Molecular biology reports · 2026Article
- A Ciliary Phosphoinositide Pathway Regulates the Dosage of Polycystins in Primary Cilia.Journal of the American Society of Nephrology : JASN · 2026Article
- Advances in the Treatment of Autosomal Dominant Polycystic Kidney Disease and Novel Therapeutic Targets.Current issues in molecular biology · 2026Review
- Spatial Transcriptomics Reveals Injured Cells, Signature Genes, and Communication Patterns in the Cyst Microenvironment of Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Article
- Epithelial Dynamics of Cystogenesis in Genetic Models of Autosomal Dominant Polycystic Kidney Disease.Cells · 2026Article
- Stratifying high-risk prediabetes clusters using blood-based epigenetic markers.Biomarker research · 2026Article
- Lack of ANKMY2 suppresses kidney cystogenesis in embryonic- and adult-onset polycystic kidney disease.PLoS genetics · 2025Article
- Extra-ciliary role for polycystins in regulation of Ezrin and renal tubular morphology.bioRxiv : the preprint server for biology · 2025Article
- Article
- A cross model spatial and single-cell atlas reveals the conserved involvement of osteopontin in polycystic kidney disease.bioRxiv : the preprint server for biology · 2025Article
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Mouse models of autosomal dominant polycystic kidney disease (ADPKD) show that intact primary cilia are required for cyst growth following the inactivation of polycystin-1. The signaling pathways underlying this process, termed cilia-dependent cyst activation (CDCA), remain unknown. Using translating ribosome affinity purification RNASeq on mouse kidneys with polycystin-1 and cilia inactivation before cyst formation, we identify the differential 'CDCA pattern' translatome specifically dysregulated in kidney tubule cells destined to form cysts. From this, Glis2 emerges as a candidate functional effector of polycystin signaling and CDCA. In vitro changes in Glis2 expression mirror the polycystin- and cilia-dependent changes observed in kidney tissue, validating Glis2 as a cell culture-based indicator of polycystin function related to cyst formation. Inactivation of Glis2 suppresses polycystic kidney disease in mouse models of ADPKD, and pharmacological targeting of Glis2 with antisense oligonucleotides slows disease progression. Glis2 transcript and protein is a functional target of CDCA and a potential therapeutic target for treating ADPKD.
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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.