ArticleJournal of biochemistry2014
aPKCλ maintains the integrity of the glomerular slit diaphragm through trafficking of nephrin to the cell surface.
Article in Journal of biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Two stress-responsive kinases suppress ferroptosis by activating antioxidant programs under mild oxidative stress.Signal transduction and targeted therapy · 2026Article
- CaNature cell biology · 2025Article
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
- An acytokinetic cell division creates PIP2-enriched membrane asymmetries leading to slit diaphragm assembly in Drosophila nephrocytes.Development (Cambridge, England) · 2023Article
- PI(4,5)P2 controls slit diaphragm formation and endocytosis in Drosophila nephrocytes.Cellular and molecular life sciences : CMLS · 2022Article
- Distinct RNA polymerase transcripts direct the assembly of phase-separated DBC1 nuclear bodies in different cell lines.Molecular biology of the cell · 2021Article
- Apical-basal polarity regulators are essential for slit diaphragm assembly and endocytosis in Drosophila nephrocytes.Cellular and molecular life sciences : CMLS · 2021Article
- Impaired NEPHRIN localization in kidney organoids derived from nephrotic patient iPS cells.Scientific reports · 2021Article
- Global transcriptomic changes occur in aged mouse podocytes.Kidney international · 2020Article
- The ubiquitin-proteasome system in kidney physiology and disease.Nature reviews. Nephrology · 2019Review
- Recent advances of animal model of focal segmental glomerulosclerosis.Clinical and experimental nephrology · 2018Review
- The phosphoinositide phosphatase Sac1 regulates cell shape and microtubule stability in the developingDevelopment (Cambridge, England) · 2018Article
- Nephrin is necessary for podocyte recovery following injury in an adult mature glomerulus.PloS one · 2018Article
- Distinct functions of Crumbs regulating slit diaphragms and endocytosis in Drosophila nephrocytes.Cellular and molecular life sciences : CMLS · 2017Article
- PACSIN2 accelerates nephrin trafficking and is up-regulated in diabetic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- A novel in vivo method to quantify slit diaphragm protein abundance in murine proteinuric kidney disease.PloS one · 2017Article
- Mature induced-pluripotent-stem-cell-derived human podocytes reconstitute kidney glomerular-capillary-wall function on a chip.Nature biomedical engineering · 2017Article
- Podocytes.F1000Research · 2016Review
- Review series: The cell biology of renal filtration.The Journal of cell biology · 2015Review
- Defects of CRB2 cause steroid-resistant nephrotic syndrome.American journal of human genetics · 2015Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The slit diaphragm (SD), the specialized intercellular junction between renal glomerular epithelial cells (podocytes), provides a selective-filtration barrier in renal glomeruli. Dysfunction of the SD results in glomerular diseases that are characterized by disappearance of SD components, such as nephrin, from the cell surface. Although the importance of endocytosis and degradation of SD components for the maintenance of SD integrity has been suggested, the dynamic nature of the turnover of intact cell-surface SD components remained unclear. Using isolated rat glomeruli we show that the turnover rates of cell-surface SD components are relatively high; they almost completely disappear from the cell surface within minutes. The exocytosis, but not endocytosis, of heterologously expressed nephrin requires the kinase activity of the cell polarity regulator atypical protein kinase C (aPKC). Consistently, we demonstrate that podocyte-specific deletion of aPKCλ resulted in a decrease of cell-surface localization of SD components, causing massive proteinuria. In conclusion, the regulation of SD turnover by aPKC is crucial for the maintenance of SD integrity and defects in aPKC signalling can lead to proteinuria. These findings not only reveal the pivotal importance of the dynamic turnover of cell-surface SD components but also suggest a novel pathophysiological basis in glomerular disease.
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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.