ArticleThe Journal of clinical investigation1997
Genetic identification of two major modifier loci of polycystic kidney disease progression in pcy mice.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 73 citations in OpenAlex.
- Molecular Pathophysiology of Autosomal Recessive Polycystic Kidney Disease.International journal of molecular sciences · 2021Review
- Modulation of polycystic kidney disease by G-protein coupled receptors and cyclic AMP signaling.Cellular signalling · 2020Review
- Disease Modeling To Understand the Pathomechanisms of Human Genetic Kidney Disorders.Clinical journal of the American Society of Nephrology : CJASN · 2020Review
- Transcriptome analysis reveals manifold mechanisms of cyst development in ADPKD.Human genomics · 2016Article
- High-resolution genetic localization of a modifying locus affecting disease severity in the juvenile cystic kidneys (jck) mouse model of polycystic kidney disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2016Article
- Endothelin 1 gene is not a major modifier of chronic kidney disease advancement among the autosomal dominant polycystic kidney disease patients.Journal of nephropharmacology · 2016Article
- Magnetic resonance microscopy of renal and biliary abnormalities in excised tissues from a mouse model of autosomal recessive polycystic kidney disease.Physiological reports · 2015Article
- Clinical and genetic characterization of a founder PKHD1 mutation in Afrikaners with ARPKD.Pediatric nephrology (Berlin, Germany) · 2015Article
- ANKS3 Co-Localises with ANKS6 in Mouse Renal Cilia and Is Associated with Vasopressin Signaling and Apoptosis In Vivo in Mice.PloS one · 2015Article
- Article
- Inhibition of Comt with tolcapone slows progression of polycystic kidney disease in the more severely affected PKD/Mhm (cy/+) substrain of the Hannover Sprague-Dawley rat.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2013Article
- Genetic background of nonmutant Piebald-Virol-Glaxo rats does not influence nephronophthisis phenotypes.International journal of nephrology and renovascular disease · 2013Article
- Loss of GM3 synthase gene, but not sphingosine kinase 1, is protective against murine nephronophthisis-related polycystic kidney disease.Human molecular genetics · 2012Article
- Genetic loci that affect aristolochic acid-induced nephrotoxicity in the mouse.American journal of physiology. Renal physiology · 2011Article
- Maternal environment interacts with modifier genes to influence progression of nephrotic syndrome.Journal of the American Society of Nephrology : JASN · 2008Article
- Loss of nephrocystin-3 function can cause embryonic lethality, Meckel-Gruber-like syndrome, situs inversus, and renal-hepatic-pancreatic dysplasia.American journal of human genetics · 2008Article
- The NPHP1 gene deletion associated with juvenile nephronophthisis is present in a subset of individuals with Joubert syndrome.American journal of human genetics · 2004Article
- Mapping modifiers affecting muscularity of the myostatin mutant (Mstn(Cmpt-dl1Abc)) compact mouse.Genetics · 2003Article
- Mutations in INVS encoding inversin cause nephronophthisis type 2, linking renal cystic disease to the function of primary cilia and left-right axis determination.Nature genetics · 2003Article
- Inversin forms a complex with catenins and N-cadherin in polarized epithelial cells.Molecular biology of the cell · 2002Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Unlike the uniform disease progression in inbred animals, polycystic kidney disease (PKD) progression within human families can be highly variable. This may be due to environmental or genetic factors or both. To determine if PKD severity can be influenced by modifier genes, we carried out an intercross between DBA/2-pcy/pcy and Mus m. castaneous involving 3,105 6-wk-old F2 mice. Large differences in PKD severity were observed in this cross. In addition, 23/ 800 phenotypically normal mice were pcy/pcy genotypically. These results demonstrated that PKD progression in pcy/ pcy mice is a quantitative trait that is strongly modulated by modifier genes. Whole genome quantitative trait loci mapping of 114 selected pcy/pcy mice (68 with the mild PKD and 46 with severe PKD) identified two loci, MOP1 and MOP2 that strongly modulate PKD progression. MOP1 (max LOD score = 10.3 at D4Mit111) and MOP2 (max LOD score = 13.8 at D16Mit1) accounted for 36.7 and 46.8% of the phenotypic variance, respectively. Two-factor ANOVA of the phenotypes and genotypes of all 673 pcy/pcy mice from our cross indicated that MOP1 and MOP2 alleles regulate PKD progression in a complex additive manner. Characterization of these novel modifying loci may provide additional insights into the pathogenesis of polycystic kidney diseases.
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