ArticleJournal of the American Society of Nephrology : JASN2015
Integration of Cistromic and Transcriptomic Analyses Identifies Nphs2, Mafb, and Magi2 as Wilms' Tumor 1 Target Genes in Podocyte Differentiation and Maintenance.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 76 citations in OpenAlex.
- MiR-423-5p inhibition alleviates podocyte apoptosis in membranous nephropathy by targeting WT1/β-catenin axis.International urology and nephrology · 2026Article
- Regulated HSPG Signaling Directs Epicardial Behavior to Support Cardiac Formation.Circulation research · 2026Article
- Upregulation of PTPRO by WT1 alleviates podocyte injury in diabetic nephropathy through inhibiting the c-Abl/p53 pathway.Cellular and molecular life sciences : CMLS · 2026Article
- FOXC2 and WT1 regulate transcriptional reprogramming during the podocyte response to injury.JCI insight · 2026Article
- Emerging genetic mechanisms of glomerular proteinuria: a podocyte-centered multi-layer network perspective.Frontiers in genetics · 2026Review
- The differential expression of MAGI2 in glomerulopathies and its application as a molecular discriminator of podocytopathies.Journal of translational medicine · 2025Article
- Principles of Zebrafish Nephron Segment Development.Journal of developmental biology · 2023Review
- Modeling Podocyte Ontogeny and Podocytopathies with the Zebrafish.Journal of developmental biology · 2023Review
- Identification of key genes and validation of key gene aquaporin 1 on Wilms' tumor metastasis.PeerJ · 2023Article
- Research progress of natural active compounds on improving podocyte function to reduce proteinuria in diabetic kidney disease.Renal failure · 2023Review
- Bioinformatics analysis and identification of genes and pathways involved in patients with Wilms tumor.Translational cancer research · 2022Article
- Alteration in DNA-binding affinity of Wilms tumor 1 protein due to WT1 genetic variants associated with steroid - resistant nephrotic syndrome in children.Scientific reports · 2022Article
- Human pluripotent stem cell-derived kidney organoids for personalized congenital and idiopathic nephrotic syndrome modeling.Development (Cambridge, England) · 2022Article
- Renal cell markers: lighthouses for managing renal diseases.American journal of physiology. Renal physiology · 2021Article
- Every Beat You Take-The Wilms' Tumor Suppressor WT1 and the Heart.International journal of molecular sciences · 2021Review
- Determination of the dynamic cellular transcriptional profiles during kidney development from birth to maturity in rats by single-cell RNA sequencing.Cell death discovery · 2021Article
- A novel WT1 gene mutation in a chinese girl with denys-drash syndrome.Journal of clinical laboratory analysis · 2021Article
- Generation of Monogenic Candidate Genes for Human Nephrotic Syndrome Using 3 Independent Approaches.Kidney international reports · 2021Article
- The Wilms Tumor GeneFrontiers in cell and developmental biology · 2021Article
- Role of miRNA-671-5p in Mediating Wnt/β-Catenin-Triggered Podocyte Injury.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Wilms' tumor suppressor gene 1 (WT1) encodes a zinc finger transcription factor. Mutation of WT1 in humans leads to Wilms' tumor, a pediatric kidney tumor, or other kidney diseases, such as Denys-Drash and Frasier syndromes. We showed previously that inactivation of WT1 in podocytes of adult mice results in proteinuria, foot process effacement, and glomerulosclerosis. However, the WT1-dependent transcriptional network regulating podocyte development and maintenance in vivo remains unknown. Here, we performed chromatin immunoprecipitation followed by high-throughput sequencing with glomeruli from wild-type mice. Additionally, we performed a cDNA microarray screen on an inducible podocyte-specific WT1 knockout mouse model. By integration of cistromic and transcriptomic analyses, we identified the WT1 targetome in mature podocytes. To further analyze the function and targets of WT1 in podocyte maturation, we used an Nphs2-Cre model, in which WT1 is deleted during podocyte differentiation. These mice display anuria and kidney hemorrhage and die within 24 hours after birth. To address the evolutionary conservation of WT1 targets, we performed functional assays using zebrafish as a model and identified Nphs2, Mafb, and Magi2 as novel WT1 target genes required for podocyte development. Our data also show that both Mafb and Magi2 are required for normal development of the embryonic zebrafish kidney. Collectively, our work provides insights into the transcriptional networks controlled by WT1 and identifies novel WT1 target genes that mediate the function of WT1 in podocyte differentiation and maintenance.
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