Reduction in numbers of nephrons or decrease in kidney function due to a variety of diseases results in compensatory renal hypertrophy (CRH). Recently, it has been proposed that CRH may be a prerequisite for progression of renal injury; genetic dissection of CRH may be therefore helpful in understanding the process whereby people with partial renal insufficiency progress to end-stage renal disease. Since genetic analysis of CRH in humans is quite limited, we searched for genetic determinants of CRH after unilateral nephrectomy using a total genome scan of the mouse BXD recombinant inbred strains. We demonstrated that CRH is a highly heritable trait and we identified a quantitative trait locus on mouse chromosome 11 near the D11Mit14 marker that exerts a major effect on CRH (lod score = 3.4) and is responsible for approximately 52% of genetic variation in CRH. This marker maps near Ace, Gh, and Ngfr positional candidate genes.

• MeSH
• hypertrofie MeSH
• kvantitativní znak dědičný * MeSH
• ledviny anatomie a histologie   patologie   MeSH
• mapování chromozomů * MeSH
• mutantní kmeny myší MeSH
• myši inbrední C57BL MeSH
• myši inbrední DBA MeSH
• myši MeSH
• nemoci ledvin genetika   patologie   MeSH
• rekombinace genetická MeSH
• velikost orgánu MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH