ArticleJournal of the American Society of Nephrology : JASN2016
Nephrin Tyrosine Phosphorylation Is Required to Stabilize and Restore Podocyte Foot Process Architecture.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 82 citations in OpenAlex.
- MCT1 as a critical regulator of insulin signaling, energy homeostasis and podocyte function.Scientific reports · 2026Article
- Afucosylated IgG in idiopathic nephrotic syndrome patients with anti-nephrin autoantibodies correlate with disease activity.Journal of translational autoimmunity · 2025Article
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Reduced nephrin tyrosine phosphorylation impairs podocyte force transmission and accelerates detachment in disease.iScience · 2025Article
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
- Anti-nephrin antibody: a potential biomarker of minimal change disease.Clinical kidney journal · 2025Article
- Digital pathology assessment of kidney glomerular filtration barrier ultrastructure in an animal model of podocytopathy.Biology methods & protocols · 2025Article
- Reduced Nephrin Tyrosine Phosphorylation Enhances Insulin Secretion and Increases Glucose Tolerance With Age.Endocrinology · 2024Article
- Minimal Change Disease: Pathogenetic Insights from Glomerular Proteomics.International journal of molecular sciences · 2024Article
- Chronic thrombotic microangiopathy presenting as acute nephrotic syndrome in a patient with renal cancer receiving tyrosine kinase inhibitor therapy.BMJ case reports · 2024Article
- The role of toll-like receptors (TLRs) and their therapeutic applications in glomerulonephritis.International urology and nephrology · 2023Review
- New Insights into the Treatment of Glomerular Diseases: When Mechanisms Become Vivid.International journal of molecular sciences · 2022Review
- Sex Differences in Glomerular Protein Expression and Effects of Soy-Based Diet on Podocyte Signaling.Canadian journal of kidney health and disease · 2022Article
- The abrupt pathological deterioration of cisplatin-induced acute kidney injury: Emerging of a critical time point.Pharmacology research & perspectives · 2021Article
- Imatinib-induced podocytopathies in a patient with gastrointestinal stromal tumor.Renal failure · 2021Article
- APOL1 risk variants and the development of HIV-associated nephropathy.The FEBS journal · 2021Review
- Nephrotoxicity of Anti-Angiogenic Therapies.Diagnostics (Basel, Switzerland) · 2021Review
- Role of Rho GTPase Interacting Proteins in Subcellular Compartments of Podocytes.International journal of molecular sciences · 2021Review
- Impaired NEPHRIN localization in kidney organoids derived from nephrotic patient iPS cells.Scientific reports · 2021Article
- Molecular Mechanisms of Proteinuria in Minimal Change Disease.Frontiers in medicine · 2021Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Podocytes are specialized epithelial cells of the kidney blood filtration barrier that contribute to permselectivity via a series of interdigitating actin-rich foot processes. Positioned between adjacent projections is a unique cell junction known as the slit diaphragm, which is physically connected to the actin cytoskeleton via the transmembrane protein nephrin. Evidence indicates that tyrosine phosphorylation of the intracellular tail of nephrin initiates signaling events, including recruitment of cytoplasmic adaptor proteins Nck1 and Nck2 that regulate actin cytoskeletal dynamics. Nephrin tyrosine phosphorylation is altered in human and experimental renal diseases characterized by pathologic foot process remodeling, prompting the hypothesis that phosphonephrin signaling directly influences podocyte morphology. To explore this possibility, we generated and analyzed knockin mice with mutations that disrupt nephrin tyrosine phosphorylation and Nck1/2 binding (nephrin(Y3F/Y3F) mice). Homozygous nephrin(Y3F/Y3F) mice developed progressive proteinuria accompanied by structural changes in the filtration barrier, including podocyte foot process effacement, irregular thickening of the glomerular basement membrane, and dilated capillary loops, with a similar but later onset phenotype in heterozygous animals. Furthermore, compared with wild-type mice, nephrin(Y3F/Y3F) mice displayed delayed recovery in podocyte injury models. Profiling of nephrin tyrosine phosphorylation dynamics in wild-type mice subjected to podocyte injury indicated site-specific differences in phosphorylation at baseline, injury, and recovery, which correlated with loss of nephrin-Nck1/2 association during foot process effacement. Our results define an essential requirement for nephrin tyrosine phosphorylation in stabilizing podocyte morphology and suggest a model in which dynamic changes in phosphotyrosine-based signaling confer plasticity to the podocyte actin cytoskeleton.
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