ArticleJournal of the American Society of Nephrology : JASN2014
Aberrant glycosylation and localization of polycystin-1 cause polycystic kidney in an AQP11 knockout model.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 citing papers in PubMed, 41 citations in OpenAlex.
- A pan-vertebrate signaling motif controls the molecular function of intracellular AQP12.The Journal of cell biology · 2026Article
- The pathophysiological significance between autosomal dominant polycystic kidney disease and neutrophil gelatinase-associated lipocalin.Kidney research and clinical practice · 2025Article
- Distinctive roles of aquaporins and novel therapeutic opportunities against cancer.RSC medicinal chemistry · 2025Review
- Mechanistic complement of autosomal dominant polycystic kidney disease: the role of aquaporins.Journal of molecular medicine (Berlin, Germany) · 2024Review
- The factory, the antenna and the scaffold: the three-way interplay between the Golgi, cilium and extracellular matrix underlying tissue function.Biology open · 2023Review
- Aquaporins in Urinary System.Advances in experimental medicine and biology · 2023Article
- Evolutionary Overview of Aquaporin Superfamily.Advances in experimental medicine and biology · 2023Article
- Classification and Gene Structure of Aquaporins.Advances in experimental medicine and biology · 2023Article
- Hyperinsulinemic Hypoglycemia Due toPediatric reports · 2022Article
- Signaling Mechanisms and Pharmacological Modulators Governing Diverse Aquaporin Functions in Human Health and Disease.International journal of molecular sciences · 2022Review
- The Role of CD147 in Pathological Cardiac Hypertrophy Is Regulated by Glycosylation.Oxidative medicine and cellular longevity · 2022Article
- Cystic kidney diseases associated with mutations in phosphomannomutase 2 promotor: a large spectrum of phenotypes.Pediatric nephrology (Berlin, Germany) · 2021Article
- Autosomal dominant polycystic kidney disease and pioglitazone for its therapy: a comprehensive review with an emphasis on the molecular pathogenesis and pharmacological aspects.Molecular medicine (Cambridge, Mass.) · 2020Review
- Inhibitors of Mammalian Aquaporin Water Channels.International journal of molecular sciences · 2019Review
- Involvement of the NADPH oxidase 2 pathway in renal oxidative stress inBiochemistry and biophysics reports · 2019Article
- Aquaporins in Renal Diseases.International journal of molecular sciences · 2019Review
- Deficient transient receptor potential vanilloid type 4 function contributes to compromised [CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Proteomic analysis of AQP11-null kidney: Proximal tubular type polycystic kidney disease.Biochemistry and biophysics reports · 2018Article
- Polycystic Kidney Disease with Hyperinsulinemic Hypoglycemia Caused by a Promoter Mutation in Phosphomannomutase 2.Journal of the American Society of Nephrology : JASN · 2017Article
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11 authors at 6 institutions in 2 countries.
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Abstract
We previously reported that disruption of the aquaporin-11 (AQP11) gene in mice resulted in cystogenesis in the kidney. In this study, we aimed to clarify the mechanism of cystogenesis in AQP11(-/-) mice. To enable the analyses of AQP11 at the protein level in vivo, AQP11 BAC transgenic mice (Tg(AQP11)) that express 3×HA-tagged AQP11 protein were generated. This AQP11 localized to the endoplasmic reticulum (ER) of proximal tubule cells in Tg(AQP11) mice and rescued renal cystogenesis in AQP11(-/-) mice. Therefore, we hypothesized that the absence of AQP11 in the ER could result in impaired quality control and aberrant trafficking of polycystin-1 (PC-1) and polycystin-2 (PC-2). Compared with kidneys of wild-type mice, AQP11(-/-) kidneys exhibited increased protein expression levels of PC-1 and decreased protein expression levels of PC-2. Moreover, PC-1 isolated from AQP11(-/-) mice displayed an altered electrophoretic mobility caused by impaired N-glycosylation processing, and density gradient centrifugation of kidney homogenate and in vivo protein biotinylation revealed impaired membrane trafficking of PC-1 in these mice. Finally, we showed that the Pkd1(+/-) background increased the severity of cystogenesis in AQP11(-/-) mouse kidneys, indicating that PC-1 is involved in the mechanism of cystogenesis in AQP11(-/-) mice. Additionally, the primary cilia of proximal tubules were elongated in AQP11(-/-) mice. Taken together, these data show that impaired glycosylation processing and aberrant membrane trafficking of PC-1 in AQP11(-/-) mice could be a key mechanism of cystogenesis in AQP11(-/-) mice.
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