ArticleKidney international2019
Corticosteroid treatment exacerbates nephrotic syndrome in a zebrafish model of magi2a knockout.
Article in Kidney international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Emerging genetic mechanisms of glomerular proteinuria: a podocyte-centered multi-layer network perspective.Frontiers in genetics · 2026Review
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- The differential expression of MAGI2 in glomerulopathies and its application as a molecular discriminator of podocytopathies.Journal of translational medicine · 2025Article
- A zebrafish model of congenital nephrotic syndrome of the Finnish type.Frontiers in cell and developmental biology · 2022Article
- Saponins fromFrontiers in pharmacology · 2022Article
- Novel zebrafish polycystic kidney disease models reveal functions of the Hippo pathway in renal cystogenesis.Disease models & mechanisms · 2021Article
- Podocyte RhoGTPases: new therapeutic targets for nephrotic syndrome?F1000Research · 2019Review
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11 authors at 1 institution in 1 country.
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Abstract
Recently, recessive mutations of MAGI2 were identified as a cause of steroid-resistant nephrotic syndrome (SRNS) in humans and mice. To further delineate the pathogenesis of MAGI2 loss of function, we generated stable knockout lines for the two zebrafish orthologues magi2a and magi2b by CRISPR/Cas9. We also developed a novel assay for the direct detection of proteinuria in zebrafish independent of transgenic background. Whereas knockout of magi2b did not yield a nephrotic syndrome phenotype, magi2a
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Registered trials
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