ArticleMolecular and cellular biology2016
Shp2 Associates with and Enhances Nephrin Tyrosine Phosphorylation and Is Necessary for Foot Process Spreading in Mouse Models of Podocyte Injury.
Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- The role of classical protein tyrosine phosphatases in diabetic kidney disease and therapeutic implications.Journal of biomedical science · 2026Review
- Mapping of PTP1B, TCPTP, SHP2, and Putative Substrates Reveals Novel Networks in Glomerular Podocytes.Journal of cellular physiology · 2026Article
- Article
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
- The integrin repertoire drives YAP-dependent epithelial:stromal interactions during injury of the kidney glomerulus.Nature communications · 2025Article
- Reduced Nephrin Tyrosine Phosphorylation Enhances Insulin Secretion and Increases Glucose Tolerance With Age.Endocrinology · 2024Article
- Protein tyrosine phosphatase 1B is a regulator of alpha-actinin4 in the glomerular podocyte.Biochimica et biophysica acta. Molecular cell research · 2024Article
- Deficiency of the Src homology phosphatase 2 in podocytes is associated with renoprotective effects in mice under hyperglycemia.Cellular and molecular life sciences : CMLS · 2022Article
- Pulmonary surfactants and the respiratory-renal connection in steroid-sensitive nephrotic syndrome of childhood.iScience · 2022Article
- Human pluripotent stem cell-derived kidney organoids for personalized congenital and idiopathic nephrotic syndrome modeling.Development (Cambridge, England) · 2022Article
- Metformin Protects against Podocyte Injury in Diabetic Kidney Disease.Pharmaceuticals (Basel, Switzerland) · 2020Review
- SHP2 inhibitor PHPS1 ameliorates acute kidney injury by Erk1/2-STAT3 signaling in a combined murine hemorrhage followed by septic challenge model.Molecular medicine (Cambridge, Mass.) · 2020Article
- Tyrosine Phosphorylation of CD2AP Affects Stability of the Slit Diaphragm Complex.Journal of the American Society of Nephrology : JASN · 2019Article
- SHROOM3-FYN Interaction Regulates Nephrin Phosphorylation and Affects Albuminuria in Allografts.Journal of the American Society of Nephrology : JASN · 2018Article
- ShcA Adaptor Protein Promotes Nephrin Endocytosis and Is Upregulated in Proteinuric Nephropathies.Journal of the American Society of Nephrology : JASN · 2018Article
- Nephrin is necessary for podocyte recovery following injury in an adult mature glomerulus.PloS one · 2018Article
- Nephrin Signaling in the Podocyte: An Updated View of Signal Regulation at the Slit Diaphragm and Beyond.Frontiers in endocrinology · 2018Review
- Molecular Mechanisms of Proteinuria in Focal Segmental Glomerulosclerosis.Frontiers in medicine · 2018Review
- Protein tyrosine phosphatase 1B deficiency in podocytes mitigates hyperglycemia-induced renal injury.Metabolism: clinical and experimental · 2017Article
- Nephron, Wilms' tumor-1 (WT1), and synaptopodin expression in developing podocytes of mice.Experimental animals · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
In most forms of glomerular diseases, loss of size selectivity by the kidney filtration barrier is associated with changes in the morphology of podocytes. The kidney filtration barrier is comprised of the endothelial lining, the glomerular basement membrane, and the podocyte intercellular junction, or slit diaphragm. The cell adhesion proteins nephrin and neph1 localize to the slit diaphragm and transduce signals in a Src family kinase Fyn-mediated tyrosine phosphorylation-dependent manner. Studies in cell culture suggest nephrin phosphorylation-dependent signaling events are primarily involved in regulation of actin dynamics and lamellipodium formation. Nephrin phosphorylation is a proximal event that occurs both during development and following podocyte injury. We hypothesized that abrogation of nephrin phosphorylation following injury would prevent nephrin-dependent actin remodeling and foot process morphological changes. Utilizing a biased screening approach, we found nonreceptor Src homology 2 (sh2) domain-containing phosphatase Shp2 to be associated with phosphorylated nephrin. We observed an increase in nephrin tyrosine phosphorylation in the presence of Shp2 in cell culture studies. In the human glomerulopathies minimal-change nephrosis and membranous nephropathy, there is an increase in Shp2 phosphorylation, a marker of increased Shp2 activity. Mouse podocytes lacking Shp2 do not develop foot process spreading when subjected to podocyte injury in vivo using protamine sulfate or nephrotoxic serum (NTS). In the NTS model, we observed a lack of foot process spreading in mouse podocytes with Shp2 deleted and smaller amounts of proteinuria. Taken together, these results suggest that Shp2-dependent signaling events are necessary for changes in foot process structure and function following injury.
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