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pubmed-article:7723240pubmed:abstractTextIn the course of studying the genetics of chlorambucil mutagenesis, we have uncovered a new model for autosomal polycystic kidney disease (PKD). In the homozygous condition, the gene, jcpk, causes a very severe disease characterized by cysts in all segments of the nephron. Death usually occurs before 10 days of age. Extrarenal involvement was also noted; enlarged bile ducts, pancreatic ducts, and gall bladder often accompanied the PKD. In addition, approximately 25% of the aged +/jcpk heterozygotes show evidence of glomerulocystic disease. This gene maps to Chromosome 10 between two DNA markers, D10Mit20 and D10Mit42. Because this gene causes extrarenal abnormalities and because it has a heterozygote effect, it may be an informative animal model for the commonly occurring human adult dominant PKD.lld:pubmed
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pubmed-article:7723240pubmed:articleTitleNew mouse model for polycystic kidney disease with both recessive and dominant gene effects.lld:pubmed
pubmed-article:7723240pubmed:affiliationMolecular Genetics Program, Wadsworth Center, New York State Department of Health, Albany, USA.lld:pubmed
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pubmed-article:7723240pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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