ArticleKidney international2015
Alternatively spliced isoforms of WT1 control podocyte-specific gene expression.
Article in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 59 citations in OpenAlex.
- 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
- Enhanced WWP2 Exacerbates Podocyte Injury in Lupus Nephritis through Monoubiquitylating H2A at K119.International journal of biological sciences · 2026Article
- New Discoveries in Podocyte Mechanosensing and Mechanotransduction.Journal of the American Society of Nephrology : JASN · 2025Article
- Podocyte dysfunction driven by heme in sickle-cell nephropathy.Scientific reports · 2025Article
- The differential expression of MAGI2 in glomerulopathies and its application as a molecular discriminator of podocytopathies.Journal of translational medicine · 2025Article
- Alternative Splicing in Mechanically Stretched Podocytes as a Model of Glomerular Hypertension.Journal of the American Society of Nephrology : JASN · 2025Article
- Mechanisms of podocyte injury in genetic kidney disease.Pediatric nephrology (Berlin, Germany) · 2025Review
- A review of the genetic background in complicated WT1-related disorders.Clinical and experimental nephrology · 2025Review
- Transplantation of decellularized porcine kidney grafts repopulated with primary human cells demonstrates filtration function in pigs.Communications medicine · 2024Article
- High-Throughput Splicing Assays Identify Known and NovelKidney international reports · 2023Article
- WT1 complete gonadal dysgenesis with membranoproliferative glomerulonephritis: case series and literature review.Pediatric nephrology (Berlin, Germany) · 2022Review
- Recessive, gain-of-function toxicity in an APOL1 BAC transgenic mouse model mirrors human APOL1 kidney disease.Disease models & mechanisms · 2021Article
- Review
- Super-Enhancer-Associated Transcription Factors Maintain Transcriptional Regulation in Mature Podocytes.Journal of the American Society of Nephrology : JASN · 2021Article
- Generation of Monogenic Candidate Genes for Human Nephrotic Syndrome Using 3 Independent Approaches.Kidney international reports · 2021Article
- Single-Cell RNA Sequencing Reveals mRNA Splice Isoform Switching during Kidney Development.Journal of the American Society of Nephrology : JASN · 2020Article
- Loss of Roundabout Guidance Receptor 2 (Robo2) in Podocytes Protects Adult Mice from Glomerular Injury by Maintaining Podocyte Foot Process Structure.The American journal of pathology · 2020Article
- The Protective Effect of Shen Qi Wan on Adenine-Induced Podocyte Injury.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Kidney organoids: accurate models or fortunate accidents.Genes & development · 2019Review
- Disruption of MAGI2-RapGEF2-Rap1 signaling contributes to podocyte dysfunction in congenital nephrotic syndrome caused by mutations in MAGI2.Kidney international · 2019Article
Corrections and comments
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Authors and funding
12 authors at 9 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Wilms' tumor suppressor WT1 is a key regulator of podocyte function that is mutated in Denys-Drash and Frasier syndromes. Here we have used an integrative approach employing ChIP, exon array, and genetic analyses in mice to address general and isoform-specific functions of WT1 in podocyte differentiation. Analysis of ChIP-Seq data showed that almost half of the podocyte-specific genes are direct targets of WT1. Bioinformatic analysis further identified coactivator FOXC1-binding sites in proximity to WT1-bound regions, thus supporting coordinated action of these transcription factors in regulating podocyte-specific genes. Transcriptional profiling of mice lacking the WT1 alternative splice isoform (+KTS) had a more restrictive set of genes whose expression depends on these alternatively spliced isoforms. One of these genes encodes the membrane-associated guanylate kinase MAGI2, a protein that localizes to the base of the slit diaphragm. Using functional analysis in mice, we further show that MAGI2α is essential for proper localization of nephrin and the assembly of the slit diaphragm complex. Finally, a dramatic reduction of MAGI2 was found in an LPS mouse model of glomerular injury and in genetic cases of human disease. Thus, our study highlights the central role of WT1 in podocyte differentiation, identifies that WT1 has a central role in podocyte differentiation, and identifies MAGI2α as the crucial isoform in slit diaphragm assembly, suggesting a causative role of this gene in the etiology of glomerular disorders.
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