ArticlePloS one2013
Aqp5 is a new transcriptional target of Dot1a and a regulator of Aqp2.
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 35 papers.
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Who cites it
35 citing papers in PubMed, 58 citations in OpenAlex.
- Regulation of renal aquaporins: implications in tubular epithelial integrity.Biochemical Society transactions · 2026Review
- Histone methylation of kidney disease: fact or fantasy?Renal failure · 2025Review
- Exploring Aquaporins in Human Studies: Mechanisms and Therapeutic Potential in Critical Illness.Life (Basel, Switzerland) · 2024Review
- A novel role of DOT1L in kidney diseases.Molecular biology reports · 2023Review
- Aquaporin-5 Dynamic Regulation.International journal of molecular sciences · 2023Review
- Forensic Diagnosis of Freshwater or Saltwater Drowning Using the Marker Aquaporin 5: An Immunohistochemical Study.Medicina (Kaunas, Lithuania) · 2022Article
- Insight into the Mammalian Aquaporin Interactome.International journal of molecular sciences · 2022Review
- Emerging roles for AQP in mammalian extracellular vesicles.Biochimica et biophysica acta. Biomembranes · 2022Review
- Protein Methylation in Diabetic Kidney Disease.Frontiers in medicine · 2022Review
- Connecting the DOTs on Cell Identity.Frontiers in cell and developmental biology · 2022Review
- The Role and Mechanism of Lysine Methyltransferase and Arginine Methyltransferase in Kidney Diseases.Frontiers in pharmacology · 2022Review
- Streptozotocin induces alpha-2u globulin nephropathy in male rats during diabetic kidney disease.BMC veterinary research · 2021Article
- Epigenetics in kidney diseases.Advances in clinical chemistry · 2021Review
- Human Aquaporins: Functional Diversity and Potential Roles in Infectious and Non-infectious Diseases.Frontiers in genetics · 2021Review
- Review
- Loss of Histone H3 K79 Methyltransferase Dot1l Facilitates Kidney Fibrosis by Upregulating Endothelin 1 through Histone Deacetylase 2.Journal of the American Society of Nephrology : JASN · 2020Article
- Pituitary Hormones (FSH, LH, PRL, and GH) Differentially Regulate AQP5 Expression in Porcine Ovarian Follicular Cells.International journal of molecular sciences · 2019Article
- Urinary AQP5 is independently associated with eGFR decline in patients with type 2 diabetes and nephropathy.Diabetes research and clinical practice · 2019Article
- Aquaporins in Renal Diseases.International journal of molecular sciences · 2019Review
- Histone Methyltransferases as Therapeutic Targets for Kidney Diseases.Frontiers in pharmacology · 2019Review
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 3 countries.
Funding
Abstract
Dot1l encodes histone H3 K79 methyltransferase Dot1a. Mice with Dot1l deficiency in renal Aqp2-expressing cells (Dot1l(AC)) develop polyuria by unknown mechanisms. Here, we report that Aqp5 links Dot1l deletion to polyuria through Aqp2. cDNA array analysis revealed and real-time RT-qPCR validated Aqp5 as the most upregulated gene in Dot1l(AC) vs. control mice. Aqp5 protein is barely detectable in controls, but robustly expressed in the Dot1l(AC) kidneys, where it colocalizes with Aqp2. The upregulation of Aqp5 is coupled with reduced association of Dot1a and H3 dimethyl K79 with specific subregions in Aqp5 5' flanking region in Dot1l(AC) vs. control mice. In vitro studies in IMCD3, MLE-15 and 293Tcells using multiple approaches including real-time RT-qPCR, luciferase reporter assay, cell surface biotinylation assay, colocalization, and co-immunoprecipitation uncovered that Dot1a represses Aqp5. Human AQP5 interacts with AQP2 and impairs its cell surface localization. The AQP5/AQP2 complex partially resides in the ER/Golgi. Consistently, AQP5 is expressed in none of 15 normal controls, but in all of 17 kidney biopsies from patients with diabetic nephropathy. In the patients with diabetic nephropathy, AQP5 colocalizes with AQP2 in the perinuclear region and AQP5 expression is associated with impaired cellular H3 dimethyl K79. Taken together, these data for the first time identify Aqp5 as a Dot1a potential transcriptional target, and an Aqp2 binding partner and regulator, and suggest that the upregulated Aqp5 may contribute to polyuria, possibly by impairing Aqp2 membrane localization, in Dot1l(AC) mice and in patients with diabetic nephropathy.
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Registered trials
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.