ArticleThe Journal of clinical investigation2009
Inactivation of Notch signaling in the renal collecting duct causes nephrogenic diabetes insipidus in mice.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed.
- Hmx2 and Dmrt2 Coordinate the Differentiation of Intercalated Cell Subtypes in Kidney.Journal of the American Society of Nephrology : JASN · 2026Article
- Dmrt2 and Hmx2 direct intercalated cell diversity in the mammalian kidney through antagonistic and supporting regulatory processes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Developmental and Cell Fate Analyses Support a Postnatal Origin for the Cortical Collecting System in the Mouse Kidney.Journal of the American Society of Nephrology : JASN · 2025Article
- Environmental and molecular control of tissue-specific ionocyte differentiation in zebrafish.Development (Cambridge, England) · 2024Article
- Notch activation defines immune-suppressive subsets of ccRCCs with unfavorable benefits from immunotherapy over VEGFR/mTOR inhibitors.iScience · 2024Article
- Environmental and molecular control of tissue-specific ionocyte differentiation in zebrafish.bioRxiv : the preprint server for biology · 2024Article
- Absence of E-Cadherin and β-Catenin in the Basal Plasma Membrane of Collecting Duct Cells During NDI Development and Recovery.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023Article
- Review
- The transcription factor Foxi1 promotes expression of V-ATPase and Gpr116 in M-1 cells.American journal of physiology. Renal physiology · 2023Article
- Cystic Fibrosis and the Cells of the Airway Epithelium: What Are Ionocytes and What Do They Do?Annual review of pathology · 2022Review
- Article
- Renal cystic disease in tuberous sclerosis complex.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Generation of patterned kidney organoids that recapitulate the adult kidney collecting duct system from expandable ureteric bud progenitors.Nature communications · 2021Article
- Review
- Kidney intercalated cells and the transcription factor FOXi1 drive cystogenesis in tuberous sclerosis complex.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Mechanisms of Cellular Plasticity in Collecting Duct Cells: Intermediate Cell Type and Notch-mediated Transdifferentiation.Function (Oxford, England) · 2021Article
- Loss of Adam10 Disrupts Ion Transport in Immortalized Kidney Collecting Duct Cells.Function (Oxford, England) · 2021Article
- Human Pluripotent Stem Cell-Derived Kidney Organoids with Improved Collecting Duct Maturation and Injury Modeling.Cell reports · 2020Article
- Foxi1 inactivation rescues loss of principal cell fate selection in Hes1-deficient kidneys but does not ensure maintenance of principal cell gene expression.Developmental biology · 2020Article
- Adaptive response of the murine collecting duct to alkali loading.Pflugers Archiv : European journal of physiology · 2020Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors.
Funding
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Abstract
The heterogeneous cellular composition of the mammalian renal collecting duct enables regulation of fluid, electrolytes, and acid-base homeostasis, but the molecular mechanism of its development has yet to be elucidated. The Notch signaling pathway is involved in cell fate determination and has been implicated in proximal-distal patterning in the mammalian kidney. To investigate the role of Notch signaling in renal collecting duct development, we generated mice in which Mind bomb-1 (Mib1), an E3 ubiquitin ligase required for the initiation of Notch signaling, was specifically inactivated in the ureteric bud of the developing kidney. Mice lacking Mib1 in the renal collecting duct displayed increased urinary production, decreased urinary osmolality, progressive hydronephrosis, sodium wasting, and a severe urinary concentrating defect manifested as nephrogenic diabetes insipidus. Histological analysis revealed a diminished number of principal cells and corresponding increase in the number of intercalated cells. Transgenic overexpression of Notch intracellular domain reversed the altered cellular composition of mutant renal collecting duct, with principal cells occupying the entire region. Our data demonstrate that Notch signaling is required for the development of the mammalian renal collecting duct and principal cell differentiation and indicate that pathway dysregulation may contribute to distal renal tubular disorders.
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