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Deficiency of the tensin2 gene in the ICGN mouse: an animal model for congenital nephrotic syndrome

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タイトル: Deficiency of the tensin2 gene in the ICGN mouse: an animal model for congenital nephrotic syndrome
著者: Cho, A-Ri 著作を一覧する
Uchio-Yamada, Kozue 著作を一覧する
Torigai, Takeshi 著作を一覧する
Miyamoto, Tomomi 著作を一覧する
Miyoshi, Ichiro 著作を一覧する
Matsuda, Junichiro 著作を一覧する
Kurosawa, Tsutomu 著作を一覧する
Kon, Yasuhiro 著作を一覧する
Asano, Atsushi 著作を一覧する
Sasaki, Nobuya 著作を一覧する
Agui, Takashi 著作を一覧する
発行日: 2006年 5月 1日
出版者: Springer
誌名: Mammalian Genome
巻: 17
号: 5
開始ページ: 407
終了ページ: 416
出版社 DOI: 10.1007/s00335-005-0167-z
抄録: 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.
Rights: © Springer
資料タイプ: article (author version)
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 安居院 高志


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