ArticleThe American journal of pathology2001
Failure of ureteric bud invasion: a new model of renal agenesis in mice.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Frem2 knockout mice exhibit Fraser syndrome phenotypes and neonatal lethality due to bilateral renal agenesis.Scientific reports · 2025Article
- Article
- Spontaneous one-kidney rats are more susceptible to develop hypertension by DOCA-NaCl and subsequent kidney injury compared with uninephrectomized rats.American journal of physiology. Renal physiology · 2016Article
- Nephron Deficiency and Predisposition to Renal Injury in a Novel One-Kidney Genetic Model.Journal of the American Society of Nephrology : JASN · 2015Article
- Radiological seminal vesicle stones may actually be in the ureter.Indian journal of urology : IJU : journal of the Urological Society of India · 2013Article
- The unilateral urogenital anomalies (UUA) rat: a new mutant strain associated with unilateral renal agenesis, cryptorchidism, and malformations of reproductive organs restricted to the left side.Comparative medicine · 2009Article
- Bilateral renal agenesis in an alpaca cria.The Canadian veterinary journal = La revue veterinaire canadienne · 2006Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FUBI (failure of ureteric bud invasion) is a highly inbred strain of mouse with a high spontaneous incidence of uni- or bilateral renal agenesis (60%). Bilateral renal agenesis is lethal within 2 days after birth. The primary defect of FUBI is failure of the ureteric bud to penetrate into the metanephric mesenchyme at around embryonic day 11, resulting in apoptosis of metanephric cells and leading to renal agenesis on the affected side. The metanephros seemed to be normal because co-culturing of the FUBI metanephros with homologous spinal cord induced differentiation of the rudiment, but co-culturing with the homologous ureteric bud frequently did not. Genetic analysis revealed that more than two genes were involved in this malformation and we mapped one of the modifier loci, fubi1, on chromosome 2, at approximately 65 cM from the centromere. In this region, there are two possible candidate genes, Wilms' tumor 1 and formin, that play important roles in kidney development. Some of formin mutants shared a similar phenotype with FUBI; however, there was no difference in the expression of formin in embryonic kidneys between FUBI and control NFS/N mice. Studies of fubi1 congenic mice indicated that interaction of two or more loci is essential for the FUBI phenotype.
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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.