ArticleProceedings of the National Academy of Sciences of the United States of America2014
MAGI-2 scaffold protein is critical for kidney barrier function.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
- Single-Nucleus Transcriptomic Atlas Reveals Disease-Associated Cellular States in Human Glomerular Diseases.Kidney international reports · 2026Article
- Disease-driven post-transcriptional alterations and alternative splicing in podocytes in focal segmental glomerulosclerosis.EMBO molecular medicine · 2026Article
- Article
- 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
- Mapping the transcriptional and epigenetic landscape of organotypic endothelial diversity in the developing and adult mouse.Nature cardiovascular research · 2025Article
- Barrier genes are associated with preterm birth.Frontiers in medicine · 2025Article
- S-SCAM is essential for synapse formation.Frontiers in cellular neuroscience · 2023Article
- Bayesian mixed model analysis uncovered 21 risk loci for chronic kidney disease in boxer dogs.PLoS genetics · 2023Article
- Immune Cell Networks Uncover Candidate Biomarkers of Melanoma Immunotherapy Response.Journal of personalized medicine · 2022Article
- Genetic variants of SDCCAG8 and MAGI2 in mitosis-related pathway genes are independent predictors of cutaneous melanoma-specific survival.Cancer science · 2021Article
- Review
- Review
- The Biological Significance and Implications of Planar Cell Polarity for Nephrology.Frontiers in physiology · 2021Review
- Article
- Review
- High tumor mutation burden is associated with DNA damage repair gene mutation in breast carcinomas.Diagnostic pathology · 2020Article
- Disruption of MAGI2-RapGEF2-Rap1 signaling contributes to podocyte dysfunction in congenital nephrotic syndrome caused by mutations in MAGI2.Kidney international · 2019Article
- Corticosteroid treatment exacerbates nephrotic syndrome in a zebrafish model of magi2a knockout.Kidney international · 2019Article
- A genome scan for genes underlying adult body size differences between Central African hunter-gatherers and farmers.Human genetics · 2018Article
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 1 country.
Funding
Abstract
MAGUK Inverted 2 (MAGI-2) is a PTEN-interacting scaffold protein implicated in cancer on the basis of rare, recurrent genomic translocations and deletions in various tumors. In the renal glomerulus, MAGI-2 is exclusively expressed in podocytes, specialized cells forming part of the glomerular filter, where it interacts with the slit diaphragm protein nephrin. To further explore MAGI-2 function, we generated Magi-2-KO mice through homologous recombination by targeting an exon common to all three alternative splice variants. Magi-2 null mice presented with progressive proteinuria as early as 2 wk postnatally, which coincided with loss of nephrin expression in the glomeruli. Magi-2-null kidneys revealed diffuse podocyte foot process effacement and focal podocyte hypertrophy by 3 wk of age, as well as progressive podocyte loss. By 5.5 wk, coinciding with a near-complete loss of podocytes, Magi-2-null mice developed diffuse glomerular extracapillary epithelial cell proliferations, and died of renal failure by 3 mo of age. As confirmed by immunohistochemical analysis, the proliferative cell populations in glomerular lesions were exclusively composed of activated parietal epithelial cells (PECs). Our results reveal that MAGI-2 is required for the integrity of the kidney filter and podocyte survival. Moreover, we demonstrate that PECs can be activated to form glomerular lesions resembling a noninflammatory glomerulopathy with extensive extracapillary proliferation, sometimes resembling crescents, following rapid and severe podocyte loss.
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