ArticlePloS one2013
A novel domain regulating degradation of the glomerular slit diaphragm protein podocin in cell culture systems.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Podocin oligomers regulate the ordering of nephrin chains, providing the molecular basis ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Integrated Functional Genomic Analysis Enables Annotation of Kidney Genome-Wide Association Study Loci.Journal of the American Society of Nephrology : JASN · 2019Article
- Endoplasmic reticulum-retained podocin mutants are massively degraded by the proteasome.The Journal of biological chemistry · 2018Article
- Sorting Nexin 9 facilitates podocin endocytosis in the injured podocyte.Scientific reports · 2017Article
- Endocytic Trafficking at the Mature Podocyte Slit Diaphragm.Frontiers in pediatrics · 2017Review
- The ubiquitin ligase Ubr4 controls stability of podocin/MEC-2 supercomplexes.Human molecular genetics · 2016Article
- Podocin is translocated to cytoplasm in puromycin aminonucleoside nephrosis rats and in poor-prognosis patients with IgA nephropathy.Cell and tissue research · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the gene NPHS2 are the most common cause of hereditary steroid-resistant nephrotic syndrome. Its gene product, the stomatin family member protein podocin represents a core component of the slit diaphragm, a unique structure that bridges the space between adjacent podocyte foot processes in the kidney glomerulus. Dislocation and misexpression of slit diaphragm components have been described in the pathogenesis of acquired and hereditary nephrotic syndrome. However, little is known about mechanisms regulating cellular trafficking and turnover of podocin. Here, we discover a three amino acids-comprising motif regulating intracellular localization of podocin in cell culture systems. Mutations of this motif led to markedly reduced degradation of podocin. These findings give novel insight into the molecular biology of the slit diaphragm protein podocin, enabling future research to establish the biological relevance of podocin turnover and localization.
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Registered trials
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