Document Detail


Loss of ICAT gene function leads to arrest of ureteric bud branching and renal agenesis.
MedLine Citation:
PMID:  17803964     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
ICAT, inhibitor of beta-catenin and T cell factor, or Ctnnbip1, is a negative regulator of the Wnt signaling pathway that interferes with the interaction between beta-catenin and T cell factor. Some ICAT-deficient (ICAT-/-) embryos exhibit unilateral or bilateral renal agenesis. In this study, we investigated developmental processes in the ICAT-/- kidney. ICAT was highly expressed in both the ureteric bud (UB) and the surrounding metanephric mesenchymal (MM) cells in the metanephros of embryonic day E11.5-E13.5 wild-type (ICAT+/+) mouse. In the E12.5-ICAT-/- metanephros, UB branching was delayed, and a T-shaped, bifurcated UB was frequently seen; this was never seen in the E12.5-ICAT+/+ metanephros. More apoptotic MM cells were detected in the ICAT-/- metanephros than in the ICAT+/+ metanephros. These results suggest that the loss of ICAT gene function causes the arrest of UB branching and the apoptotic death of MM cells, resulting in renal agenesis.
Authors:
Yoshimi Hasegawa; Kiyotoshi Satoh; Akiko Iizuka-Kogo; Atsushi Shimomura; Ryuji Nomura; Tetsu Akiyama; Takao Senda
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-08-27
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  362     ISSN:  0006-291X     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2007 Nov 
Date Detail:
Created Date:  2007-09-18     Completed Date:  2007-12-13     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  988-94     Citation Subset:  IM    
Affiliation:
Department of Anatomy I, Fujita Health University School of Medicine, Toyoake, Aichi 470-1192, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Cycle Proteins / metabolism*
Embryonic Development*
Kidney / abnormalities*,  embryology,  metabolism*
Mice
Mice, Knockout
Morphogenesis*
Transcription Factors / metabolism*
Ureter / abnormalities*,  embryology,  metabolism*
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 0/ICAT protein, mouse; 0/Transcription Factors

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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