Deficiency of the tensin2 gene in the ICGN mouse: an animal model for congenital nephrotic syndrome
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概要
- 論文の詳細を見る
The ICGN mouse is a model for nephrotic syndrome (NS) which presents with proteinuria, hyperlipidemia, and edema. In this study we attempted to identify the gene(s) responsible for NS. By analyzing albuminuria in 160 (ICGN × MSM)F1 × ICGN backcross progenies, we found that NS in the ICGN mouse is caused by more than one gene. We then performed a quantitative trait locus (QTL) analysis and detected a QTL with a very high LOD score peak in the telomeric region of Chr 15. By analyzing the nucleotide sequence of 22 genes located close to the QTL, we found that the tensin2 gene of the ICGN mouse possessed an 8-nucleotide deletion mutation in exon 18, leading to a frameshift and giving rise to a terminal codon at a premature position. Analyses of in situ hybridization and immunohistochemistry revealed that tensin2 was expressed in podocytes and tubular epithelial cells in normal mice but not in the ICGN mouse. These data raise the possibility that a mutation of the tensin2 gene is responsible for NS of the ICGN mouse and tensin2 is a prerequisite for the normal kidney function.
- Springerの論文
- 2006-05-01
著者
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Asano Atsushi
Laboratory Of Experimental Animal Science Graduate School Of Veterinary Medicine Hokkaido University
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Asano Atsushi
Mobile Computing And Communications Development Center Digital Media Equipment And Services Company
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Asano Atsushi
北海道大学 獣医学研究科動物疾病制御学講座実験動物学
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Tachi Atsushi
Laboratory Of Public Health Graduate School Of Veterinary Medicine Hokkaido University
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Agui T
Laboratory Of Laboratory Animal Science And Medicine Department Of Disease Control Graduate School O
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Kon Yasuhiro
Laboratory Of Anatomy Department Of Biomedical Sciences Graduate School Of Veterinary Medicine Hokka
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