ArticleThe Journal of clinical investigation2000
Generation and phenotype of mice harboring a nonsense mutation in the V2 vasopressin receptor gene.
Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 118 citations in OpenAlex.
- Construction of arginine vasopressin receptor 2-deficient rats by the rGONAD method.Clinical and experimental nephrology · 2025Article
- Metabolic effects of vasopressin in pathophysiology of diabetic kidney disease.Frontiers in endocrinology · 2023Review
- LRBA is essential for urinary concentration and body water homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Novel AVPR2 mutations and clinical characteristics in 28 Chinese families with congenital nephrogenic diabetes insipidus.Journal of endocrinological investigation · 2021Article
- Hepsin-mediated Processing of Uromodulin is Crucial for Salt-sensitivity and Thick Ascending Limb Homeostasis.Scientific reports · 2019Article
- Preeclampsia-Like Features and Partial Lactation Failure in Mice Lacking Cystathionine γ-Lyase-An Animal Model of Cystathioninuria.International journal of molecular sciences · 2019Article
- Mechanisms of Developmental Toxicity of Dioxins and Related Compounds.International journal of molecular sciences · 2019Review
- Regulation of Inflammatory Functions of Macrophages and T Lymphocytes by NFAT5.Frontiers in immunology · 2019Review
- Hereditary Nephrogenic Diabetes Insipidus: Pathophysiology and Possible Treatment. An Update.International journal of molecular sciences · 2017Review
- Unraveling the Physiology of (Pro)Renin Receptor in the Distal Nephron.Hypertension (Dallas, Tex. : 1979) · 2017Review
- Context-dependent regulation of Th17-associated genes and IFNγ expression by the transcription factor NFAT5.Immunology and cell biology · 2017Article
- AKAP220 manages apical actin networks that coordinate aquaporin-2 location and renal water reabsorption.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- A novel therapeutic effect of statins on nephrogenic diabetes insipidus.Journal of cellular and molecular medicine · 2015Review
- Nephrogenic diabetes insipidus: essential insights into the molecular background and potential therapies for treatment.Endocrine reviews · 2013Review
- Congenital nephrogenic diabetes insipidus: the current state of affairs.Pediatric nephrology (Berlin, Germany) · 2012Review
- Aquaporin 2 promotes cell migration and epithelial morphogenesis.Journal of the American Society of Nephrology : JASN · 2012Article
- Central diabetes insipidus associated with impaired renal aquaporin-1 expression in mice lacking liver X receptor β.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Transgenic overexpression of p23 induces spontaneous hydronephrosis in mice.International journal of experimental pathology · 2011Article
- Identification of SPRED2 (sprouty-related protein with EVH1 domain 2) as a negative regulator of the hypothalamic-pituitary-adrenal axis.The Journal of biological chemistry · 2011Article
- AVR/NAVR deficiency lowers blood pressure and differentially affects urinary concentrating ability, cognition, and anxiety-like behavior in male and female mice.Physiological genomics · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 7 institutions in 4 countries.
Funding
Abstract
The V2 vasopressin receptor (V2R) plays a key role in the maintenance of a normal body water balance. To generate an in vivo model that allows the physiological and molecular analysis of the role of V2Rs in kidney function, we have created mouse lines that lack functional V2Rs by using targeted mutagenesis in mouse embryonic stem cells. Specifically, we introduced a nonsense mutation known to cause X-linked nephrogenic diabetes insipidus (XNDI) in humans (Glu242stop) into the mouse genome. V2R-deficient hemizygous male pups showed a decrease in basal urine osmolalities and were unable to concentrate their urine. These pups also exhibited an enlargement of renal pelvic space, failed to thrive, and died within the first week after birth due to hypernatremic dehydration. Interestingly, female mice heterozygous for the V2R mutation showed normal growth but displayed an XNDI-like phenotype, characterized by reduced urine concentrating ability of the kidney, polyuria, and polydipsia. Western blot analysis and immunoelectron microscopic studies showed that the loss of functional V2Rs had no significant effect on the basal expression levels of aquaporin-2 and the bumetanide-sensitive Na-K-2Cl cotransporter (BSC-1). The V2R mutant mice described here should serve as highly useful tools for the development of novel therapeutic strategies for the treatment of XNDI.
Indexed as
Identifiers
What OpenQuestion holds
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.