ArticleMolecular and cellular biology2011
Requirement for class II phosphoinositide 3-kinase C2alpha in maintenance of glomerular structure and function.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- Inactivation of PI3K-C2α deregulates cell death pathways and sensitizes to endotoxic shock.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Transcriptomic, epigenomic, and spatial metabolomic cell profiling redefines regional human kidney anatomy.Cell metabolism · 2024Article
- Article
- Phosphoinositide 3-Kinases as Potential Targets for Thrombosis Prevention.International journal of molecular sciences · 2022Review
- Steroid-sensitive nephrotic syndrome candidate gene CLVS1 regulates podocyte oxidative stress and endocytosis.JCI insight · 2022Article
- PI3K Isoforms in B Cells.Current topics in microbiology and immunology · 2022Article
- UsingFrontiers in cell and developmental biology · 2022Review
- Podocyte Endocytosis in Regulating the Glomerular Filtration Barrier.Frontiers in medicine · 2022Review
- PI(3,4)P2-mediated cytokinetic abscission prevents early senescence and cataract formation.Science (New York, N.Y.) · 2021Article
- Review
- Class II phosphatidylinositol 3-kinase isoforms in vesicular trafficking.Biochemical Society transactions · 2021Review
- Article
- Predicting human disease mutations and identifying drug targets from mouse gene knockout phenotyping campaigns.Disease models & mechanisms · 2019Review
- The transient cortical zone in the adrenal gland: the mystery of the adrenal X-zone.The Journal of endocrinology · 2019Review
- Class II PI3Ks at the Intersection between Signal Transduction and Membrane Trafficking.Biomolecules · 2019Review
- Phosphoinositides in the kidney.Journal of lipid research · 2019Review
- Article
- Podocyte-actin dynamics in health and disease.Nature reviews. Nephrology · 2016Review
- Inactivation of class II PI3K-C2α induces leptin resistance, age-dependent insulin resistance and obesity in male mice.Diabetologia · 2016Article
- Phosphoinositide 3-Kinase-C2α Regulates Polycystin-2 Ciliary Entry and Protects against Kidney Cyst Formation.Journal of the American Society of Nephrology : JASN · 2016Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
An early lesion in many kidney diseases is damage to podocytes, which are critical components of the glomerular filtration barrier. A number of proteins are essential for podocyte filtration function, but the signaling events contributing to development of nephrotic syndrome are not well defined. Here we show that class II phosphoinositide 3-kinase C2α (PI3KC2α) is expressed in podocytes and plays a critical role in maintaining normal renal homeostasis. PI3KC2α-deficient mice developed chronic renal failure and exhibited a range of kidney lesions, including glomerular crescent formation and renal tubule defects in early disease, which progressed to diffuse mesangial sclerosis, with reduced podocytes, widespread effacement of foot processes, and modest proteinuria. These findings were associated with altered expression of nephrin, synaptopodin, WT-1, and desmin, indicating that PI3KC2α deficiency specifically impacts podocyte morphology and function. Deposition of glomerular IgA was observed in knockout mice; importantly, however, the development of severe glomerulonephropathy preceded IgA production, indicating that nephropathy was not directly IgA mediated. PI3KC2α deficiency did not affect immune responses, and bone marrow transplantation studies also indicated that the glomerulonephropathy was not the direct consequence of an immune-mediated disease. Thus, PI3KC2α is critical for maintenance of normal glomerular structure and function by supporting normal podocyte function.
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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.