ArticleOncogene2001
Early development of polycystic kidney disease in transgenic mice expressing an activated mutant of the beta-catenin gene.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.
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.
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Who cites it
124 citing papers in PubMed, 236 citations in OpenAlex.
- Primary cilia: master conductors of cellular communication in development and disease.Nature reviews. Nephrology · 2026Review
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- Autosomal Dominant Polycystic Kidney Disease: From Pathogenesis to Organoid Disease Models.Biomedicines · 2025Review
- Glycogen synthase kinase 3β: a key player in progressive chronic kidney disease.Clinical science (London, England : 1979) · 2025Review
- Signal integrator function of CXXC5 in Cancer.Cell communication and signaling : CCS · 2025Review
- The Tumor-Associated Calcium Signal Transducer 2 (TACSTD2) oncogene is upregulated in cystic epithelial cells revealing a potential new target for polycystic kidney disease.PLoS genetics · 2024Article
- Article
- The Role of the PAX Genes in Renal Cell Carcinoma.International journal of molecular sciences · 2024Review
- Article
- Polycystin-2-dependent transcriptome reveals early response of autosomal dominant polycystic kidney disease.Physiological genomics · 2023Article
- Ameliorating liver disease in an autosomal recessive polycystic kidney disease mouse model.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Clinical findings, underlying pathogenetic processes and treatment of vascular dysfunction in autosomal dominant polycystic kidney disease.Renal failure · 2023Review
- Transcription factors AP-2α and AP-2β regulate distinct segments of the distal nephron in the mammalian kidney.Nature communications · 2022Article
- Primary cilium in kidney development, function and disease.Frontiers in endocrinology · 2022Review
- Kidney epithelial targeted mitochondrial transcription factor A deficiency results in progressive mitochondrial depletion associated with severe cystic disease.Kidney international · 2021Article
- TAZ/Wnt-β-catenin/c-MYC axis regulates cystogenesis in polycystic kidney disease.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- AP-2β/KCTD1 Control Distal Nephron Differentiation and Protect against Renal Fibrosis.Developmental cell · 2020Article
- A case of cerebral infarction caused by painless acute aortic dissection in autosomal dominant polycystic kidney disease.CEN case reports · 2020Article
- Review
- Hepatocyte nuclear factor-1β regulates Wnt signaling through genome-wide competition with β-catenin/lymphoid enhancer binding factor.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
64 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is common and is a major cause of renal failure. Although the genetics of ADPKD are well known and have led to the discovery of polycystins, a new protein family, the pathogenesis of the disease remains largely unknown. Recent studies have indicated that the beta-catenin signaling pathway is one of the targets of the transduction pathway controlled by the polycystins. We have generated transgenic mice that overproduce an oncogenic form of beta-catenin in the epithelial cells of the kidney. These mice developed severe polycystic lesions soon after birth that affected the glomeruli, proximal, distal tubules and collecting ducts. The phenotype of these mice mimicked the human ADPKD phenotype. Cyst formation was associated with an increase in cell proliferation and apoptosis. The cell proliferation and apoptotic indexes was increased 4-5-fold and 3-4-fold, respectively, in cystic tubules of the transgenic mice compared to that of littermate controls. Our findings provide experimental genetic evidence that activation of the Wnt/beta-catenin signaling pathway causes polycystic kidney disease and support the view that dysregulation of the Wnt/beta-catenin signaling is involved in its pathogenesis.
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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.