ArticleThe Journal of biological chemistry2009
Cyst formation in kidney via B-Raf signaling in the PKD2 transgenic mice.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 82 citations in OpenAlex.
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- Generation of transgenic pigs with targeted insertion of a wildtype copy of human PKD2 gene.Molecular biology reports · 2026Article
- A heteromeric TRP channel that functions as a WNT-activated G protein-coupled receptor.Nature communications · 2026Article
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Review
- Review
- The lonidamine derivative H2-gamendazole reduces cyst formation in polycystic kidney disease.American journal of physiology. Renal physiology · 2022Article
- The critical role of the Hippo signaling pathway in kidney diseases.Frontiers in pharmacology · 2022Review
- Molecular Mechanisms of Epigenetic Regulation, Inflammation, and Cell Death in ADPKD.Frontiers in molecular biosciences · 2022Review
- Polycystin-1 dependent regulation of polycystin-2 via GRP94, a member of HSP90 family that resides in the endoplasmic reticulum.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Molecular dysregulation of ciliary polycystin-2 channels caused by variants in the TOP domain.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Proliferative signaling by ERBB proteins and RAF/MEK/ERK effectors in polycystic kidney disease.Cellular signalling · 2020Review
- Article
- Hyperactivity of Mek in TNS1 knockouts leads to potential treatments for cystic kidney diseases.Cell death & disease · 2019Article
- TRPP2 dysfunction decreases ATP-evoked calcium, induces cell aggregation and stimulates proliferation in T lymphocytes.BMC nephrology · 2019Article
- Leucine-485 deletion variant of BRAF may exhibit the severe end of the clinical spectrum of CFC syndrome.Journal of human genetics · 2019Article
- Novel long-range regulatory mechanisms controlling PKD2 gene expression.BMC genomics · 2018Article
- Structure of the polycystic kidney disease TRP channel Polycystin-2 (PC2).Nature structural & molecular biology · 2017Article
- Far Upstream Element-Binding Protein 1 Binds the 3' Untranslated Region of PKD2 and Suppresses Its Translation.Journal of the American Society of Nephrology : JASN · 2016Article
- Inhibition of histone deacetylase 6 activity reduces cyst growth in polycystic kidney disease.Kidney international · 2016Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenic mechanisms of human autosomal dominant polycystic kidney disease (ADPKD) have been well known to include the mutational inactivation of PKD2. Although haploinsufficiency and loss of heterozygosity at the Pkd2 locus can cause cyst formation in mice, polycystin-2 is frequently expressed in the renal cyst of human ADPKD, raising the possibility that deregulated activation of PKD2 may be associated with the cystogenesis of human ADPKD. To determine whether increased PKD2 expression is physiologically pathogenic, we generated PKD2-overexpressing transgenic mice. These mice developed typical renal cysts and an increase of proliferation and apoptosis, which are reflective of the human ADPKD phenotype. These manifestations were first observed at six months, and progressed with age. In addition, we found that ERK activation was induced by PKD2 overexpression via B-Raf signaling, providing a possible molecular mechanism of cystogenesis. In PKD2 transgenic mice, B-Raf/MEK/ERK sequential signaling was up-regulated. Additionally, the transgenic human polycystin-2 partially rescues the lethality of Pkd2 knock-out mice and therefore demonstrates that the transgene generated a functional product. Functional strengthening or deregulated activation of PKD2 may be a direct cause of ADPKD. The present study provides evidence for an in vivo role of overexpressed PKD2 in cyst formation. This transgenic mouse model should provide new insights into the pathogenic mechanism of human 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.