ArticleJCI insight2021
Pdcd10-Stk24/25 complex controls kidney water reabsorption by regulating Aqp2 membrane targeting.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Diurnal function and expression of aquaporins in the mouse kidney.American journal of physiology. Renal physiology · 2025Article
- Programmed Cell Death Protein 10 (PDCD10) Regulates Vesicle Trafficking and Contributes to the Progression of Clear Cell Renal Cell Carcinoma.Journal of extracellular vesicles · 2025Article
- Lysine acetylation of aquaporin-3 promotes water permeability but is not essential for urine concentrating ability.American journal of physiology. Renal physiology · 2025Article
- Multi-Omic Analysis Reveals Genetic Determinants and Therapeutic Targets of Chronic Kidney Disease and Kidney Function.International journal of molecular sciences · 2024Article
- Molecular complex detection in protein interaction networks through reinforcement learning.BMC bioinformatics · 2023Article
- Release of STK24/25 suppression on MEKK3 signaling in endothelial cells confers cerebral cavernous malformation.JCI insight · 2023Article
- Endothelial Cell-Pericyte Interactions in the Pathogenesis of Cerebral Cavernous Malformations (CCMs).Cold Spring Harbor perspectives in medicine · 2023Review
- Review
- Article
- Exosomal and Plasma Non-Coding RNA Signature Associated with Urinary Albumin Excretion in Hypertension.International journal of molecular sciences · 2022Article
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Authors and funding
17 authors at 8 institutions in 4 countries.
Funding
Abstract
PDCD10, also known as CCM3, is a gene found to be associated with the human disease cerebral cavernous malformations (CCMs). PDCD10 forms a complex with GCKIII kinases including STK24, STK25, and MST4. Studies in C. elegans and Drosophila have shown a pivotal role of the PDCD10-GCKIII complex in maintaining epithelial integrity. Here, we found that mice deficient of Pdcd10 or Stk24/25 in the kidney tubules developed polyuria and displayed increased water consumption. Although the expression levels of aquaporin genes were not decreased, the levels of total and phosphorylated aquaporin 2 (Aqp2) protein in the apical membrane of tubular epithelial cells were decreased in Pdcd10- and Stk24/25-deficient mice. This loss of Aqp2 was associated with increased expression and membrane targeting of Ezrin and phosphorylated Ezrin, Radixin, Moesin (p-ERM) proteins and impaired intracellular vesicle trafficking. Treatment with Erlotinib, a tyrosine kinase inhibitor promoting exocytosis and inhibiting endocytosis, normalized the expression level and membrane abundance of Aqp2 protein, and partially rescued the water reabsorption defect observed in the Pdcd10-deficient mice. Our current study identified the PDCD10-STK-ERM signaling pathway as a potentially novel pathway required for water balance control by regulating vesicle trafficking and protein abundance of AQP2 in the kidneys.
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