HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine >
Peer-reviewed Journal Articles, etc >

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

Files in This Item:
revised.icgn(mamm.genome).pdf4.13 MBPDFView/Open
Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/11370

Title: Deficiency of the tensin2 gene in the ICGN mouse: an animal model for congenital nephrotic syndrome
Authors: Cho, A-Ri Browse this author
Uchio-Yamada, Kozue Browse this author
Torigai, Takeshi Browse this author
Miyamoto, Tomomi Browse this author
Miyoshi, Ichiro Browse this author
Matsuda, Junichiro Browse this author
Kurosawa, Tsutomu Browse this author
Kon, Yasuhiro Browse this author →KAKEN DB
Asano, Atsushi Browse this author
Sasaki, Nobuya Browse this author →KAKEN DB
Agui, Takashi Browse this author →KAKEN DB
Issue Date: 1-May-2006
Publisher: Springer
Journal Title: Mammalian Genome
Volume: 17
Issue: 5
Start Page: 407
End Page: 416
Publisher DOI: 10.1007/s00335-005-0167-z
Abstract: 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
Relation: http://www.springerlink.com
Type: article (author version)
URI: http://hdl.handle.net/2115/11370
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 安居院 高志

Export metadata:

OAI-PMH ( junii2 , jpcoar )

MathJax is now OFF:


 

 - Hokkaido University