ArticleDiabetes2016
CIN85 Deficiency Prevents Nephrin Endocytosis and Proteinuria in Diabetes.
Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2-COL3A1 axis.Molecular oncology · 2026Article
- Nicotinamide mononucleotide protects against diabetic nephropathyWorld journal of diabetes · 2025Article
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
- A human stem cell-derived model reveals pathologic extracellular matrix remodeling in diabetic podocyte injury.Matrix biology plus · 2024Article
- Oxidative Stress Contributes to Slit Diaphragm Defects Caused by Disruption of Endocytosis.Kidney international reports · 2024Article
- U-shaped relationship between fasting blood glucose and urinary albumin-to-creatinine ratio in the general United States population.Frontiers in endocrinology · 2024Article
- Zebrafish Model to Study Podocyte Function Within the Glomerular Filtration Barrier.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Article
- Modes of podocyte death in diabetic kidney disease: an update.Journal of nephrology · 2022Review
- CARMIL3 is important for cell migration and morphogenesis during early development in zebrafish.Developmental biology · 2022Article
- Podocyte Endocytosis in Regulating the Glomerular Filtration Barrier.Frontiers in medicine · 2022Review
- The Zebrafish Model to Understand Epigenetics in Renal Diseases.International journal of molecular sciences · 2021Review
- Dysregulated Dynein-Mediated Trafficking of Nephrin Causes INF2-related Podocytopathy.Journal of the American Society of Nephrology : JASN · 2021Article
- USP36-Mediated Deubiquitination of DOCK4 Contributes to the Diabetic Renal Tubular Epithelial Cell InjuryFrontiers in cell and developmental biology · 2021Article
- Inhibiting calpain 1 and 2 in cyclin G associated kinase-knockout mice mitigates podocyte injury.JCI insight · 2020Article
- High glucose-mediated PICALM and mTORC1 modulate processing of amyloid precursor protein via endosomal abnormalities.British journal of pharmacology · 2020Article
- The Protective Effect of Shen Qi Wan on Adenine-Induced Podocyte Injury.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Overexpression of Myo1e promotes albumin endocytosis by mouse glomerular podocytes mediated by Dynamin.PeerJ · 2020Article
- Article
- Tyrosine Phosphorylation of CD2AP Affects Stability of the Slit Diaphragm Complex.Journal of the American Society of Nephrology : JASN · 2019Article
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9 authors at 3 institutions in 2 countries.
Funding
Abstract
Diabetic nephropathy (DN) is the major cause of end-stage renal disease worldwide. Podocytes are important for glomerular filtration barrier function and maintenance of size selectivity in protein filtration in the kidney. Podocyte damage is the basis of many glomerular diseases characterized by loss of interdigitating foot processes and decreased expression of components of the slit diaphragm. Nephrin, a podocyte-specific protein, is the main component of the slit diaphragm. Loss of nephrin is observed in human and rodent models of diabetic kidney disease. The long isoform of CIN85 (RukL) is a binding partner of nephrin that mediates nephrin endocytosis via ubiquitination in podocytes. Here we demonstrate that the loss of nephrin expression and the onset of proteinuria in diabetic mice correlate with an increased accumulation of ubiquitinated proteins and expression of CIN85/RukL in podocytes. CIN85/RukL deficiency preserved nephrin surface expression on the slit diaphragm and reduced proteinuria in diabetic mice, whereas overexpression of CIN85 in zebrafish induced severe edema and disruption of the filtration barrier. Thus, CIN85/RukL is involved in endocytosis of nephrin in podocytes under diabetic conditions, causing podocyte depletion and promoting proteinuria. CIN85/RukL expression therefore shows potential to be a novel target for antiproteinuric therapy in diabetes.
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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.