ArticleThe Journal of clinical investigation2012
Crk1/2-dependent signaling is necessary for podocyte foot process spreading in mouse models of glomerular disease.
Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 111 citations in OpenAlex.
- Application of the nephrotoxic serum nephritis model in glomerulonephritis research.Molecular medicine (Cambridge, Mass.) · 2026Review
- Endothelial cell-released CD93 contributes to podocyte injury in idiopathic nephrotic syndrome.Science translational medicine · 2026Article
- 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
- GIT ArfGAP2: A Cytoskeletal Safeguard in Podocytes: Suppressing Rac1 to Combat Glomerular Injury.Journal of the American Society of Nephrology : JASN · 2025Article
- Article
- VEGFA promotes the occurrence of PLA2R-associated idiopathic membranous nephropathy by angiogenesis via the PI3K/AKT signalling pathway.BMC nephrology · 2022Article
- Pulmonary surfactants and the respiratory-renal connection in steroid-sensitive nephrotic syndrome of childhood.iScience · 2022Article
- Tensin 2-deficient nephropathy: mechanosensitive nephropathy, genetic susceptibility.Experimental animals · 2022Review
- Rap1 Activity Is Essential for Focal Adhesion and Slit Diaphragm Integrity.Frontiers in cell and developmental biology · 2022Article
- Dasatinib-Induced Nephrotic Syndrome: A Case Report.Cureus · 2021Article
- α-Galactosidase a Deficiency in Fabry Disease Leads to Extensive Dysregulated Cellular Signaling Pathways in Human Podocytes.International journal of molecular sciences · 2021Article
- Role of Rho GTPase Interacting Proteins in Subcellular Compartments of Podocytes.International journal of molecular sciences · 2021Review
- Review
- Molecular Mechanisms of Proteinuria in Minimal Change Disease.Frontiers in medicine · 2021Review
- ShcA expression in podocytes is dispensable for glomerular development but its upregulation is associated with kidney disease.American journal of translational research · 2021Article
- Phosphorylation of key podocyte proteins and the association with proteinuric kidney disease.American journal of physiology. Renal physiology · 2020Review
- Review
- Deletion of the Tensin2 SH2-PTB domain, but not the loss of its PTPase activity, induces podocyte injury in FVB/N mouse strain.Experimental animals · 2020Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 8 institutions in 2 countries.
Funding
Abstract
The morphology of healthy podocyte foot processes is necessary for maintaining the characteristics of the kidney filtration barrier. In most forms of glomerular disease, abnormal filter barrier function results when podocytes undergo foot process spreading and retraction by remodeling their cytoskeletal architecture and intercellular junctions during a process known as effacement. The cell adhesion protein nephrin is necessary for establishing the morphology of the kidney podocyte in development by transducing from the specialized podocyte intercellular junction phosphorylation-mediated signals that regulate cytoskeletal dynamics. The present studies extend our understanding of nephrin function by showing that nephrin activation in cultured podocytes induced actin dynamics necessary for lamellipodial protrusion. This process required a PI3K-, Cas-, and Crk1/2-dependent signaling mechanism distinct from the previously described nephrin-Nck1/2 pathway necessary for assembly and polymerization of actin filaments. Our present findings also support the hypothesis that mechanisms governing lamellipodial protrusion in culture are similar to those used in vivo during foot process effacement in a subset of glomerular diseases. In mice, podocyte-specific deletion of Crk1/2 prevented foot process effacement in one model of podocyte injury and attenuated foot process effacement and associated proteinuria in a delayed fashion in a second model. In humans, focal adhesion kinase and Cas phosphorylation - markers of focal adhesion complex-mediated Crk-dependent signaling - was induced in minimal change disease and membranous nephropathy, but not focal segmental glomerulosclerosis. Together, these observations suggest that activation of a Cas-Crk1/2-dependent complex is necessary for foot process effacement observed in distinct subsets of human glomerular diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.