ArticleKidney international2011
The fate of Notch-deficient nephrogenic progenitor cells during metanephric kidney development.
Article in Kidney international, 2011. 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, 36 citations in OpenAlex.
- egr1 and egr4 regulate zebrafish renal regeneration by promoting foxm1 expression.Journal of molecular cell biology · 2026Article
- Controlling nephron precursor differentiation to generate proximal-biased kidney organoids with emerging maturity.Nature communications · 2025Article
- Dexamethasone induces transgenerational inheritance of fetal-derived glomerulosclerosis phenotype in offspring through GR/DNMT3a mediated alterations of the lncRNA-Meg3/Notch signaling pathway.Cell communication and signaling : CCS · 2025Article
- Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.Disease models & mechanisms · 2025Article
- Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.bioRxiv : the preprint server for biology · 2024Article
- Variants in tubule epithelial regulatory elements mediate most heritable differences in human kidney function.bioRxiv : the preprint server for biology · 2024Article
- Glucocorticoids Inhibit EGFR Signaling Activation in Podocytes in Anti-GBM Crescentic Glomerulonephritis.Frontiers in medicine · 2022Article
- Notch signaling regulates Akap12 expression and primary cilia length during renal tubule morphogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Notch Signaling in Kidney Development, Maintenance, and Disease.Biomolecules · 2019Review
- Aberrant Regulation of Notch3 Signaling Pathway in Polycystic Kidney Disease.Scientific reports · 2018Article
- Rho-Kinase Blockade Attenuates Podocyte Apoptosis by Inhibiting the Notch Signaling Pathway in Diabetic Nephropathy.International journal of molecular sciences · 2017Article
- Partitioning-Defective 1a/b Depletion Impairs Glomerular and Proximal Tubule Development.Journal of the American Society of Nephrology : JASN · 2016Article
- Review
- New insights into glomerular parietal epithelial cell activation and its signaling pathways in glomerular diseases.BioMed research international · 2015Review
- Atlas of Cellular Dynamics during Zebrafish Adult Kidney Regeneration.Stem cells international · 2015Article
- The integrin β1 subunit regulates paracellular permeability of kidney proximal tubule cells.The Journal of biological chemistry · 2014Article
- Membrane trafficking in podocyte health and disease.Pediatric nephrology (Berlin, Germany) · 2013Review
- Renal involvement and the role of Notch signalling in Alagille syndrome.Nature reviews. Nephrology · 2013Review
- Inhibition of Notch pathway attenuates the progression of human immunodeficiency virus-associated nephropathy.American journal of physiology. Renal physiology · 2013Article
- Notch signaling in diabetic nephropathy.Experimental cell research · 2012Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
To determine which nephron segments require Notch signals for development, we conditionally deleted Rbpj, a transcription factor required for canonical Notch signaling, in nephrogenic progenitors (NPs) of the metanephric mesenchyme. The retinoic acid receptor-β2 (Rarb2) promoter efficiently directed Cre-recombinase (Cre) activity to these progenitors. Conditional knockout of Rbpj in mice (Rarb2Cre(+)/Rbpj (f/-)) caused severe renal hypoplasia, as indicated by a 70-95% reduction in nephron number and the development of tubular cysts. To track the fate of NPs following Rarb2Cre expression, we labeled them with membrane-associated enhanced green fluorescent protein (GFP). In TomatoGFP(+)/Rarb2Cre(+) control mice, NPs differentiated into epithelia of all nephron segments, except into collecting ducts. In TomatoGFP(+)/Rarb2Cre(+)/Rbpj (f/-) conditional knockout mice, NPs developed into podocytes or distal tubular epithelia, indicating that canonical Notch signals were not required for mesenchymal-to-epithelial transition or for the specification of these nephron segments. Conversely, the few proximal tubules and associated cysts that developed in these mice were derived from the 5-10% of NPs that had failed to express Cre and, therefore, had intact Notch signaling. Thus, our fate mapping studies establish that the profound effect of Notch signaling on nephrogenesis is due to the specification of proximal but not distal tubules or podocytes.
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Registered trials
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