| Loss of ICAT gene function leads to arrest of ureteric bud branching and renal agenesis. | |
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MedLine Citation:
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PMID: 17803964 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Yoshimi Hasegawa; Kiyotoshi Satoh; Akiko Iizuka-Kogo; Atsushi Shimomura; Ryuji Nomura; Tetsu Akiyama; Takao Senda |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2007-08-27 |
Journal Detail:
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Title: Biochemical and biophysical research communications Volume: 362 ISSN: 0006-291X ISO Abbreviation: Biochem. Biophys. Res. Commun. Publication Date: 2007 Nov |
Date Detail:
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Created Date: 2007-09-18 Completed Date: 2007-12-13 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0372516 Medline TA: Biochem Biophys Res Commun Country: United States |
Other Details:
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Languages: eng Pagination: 988-94 Citation Subset: IM |
Affiliation:
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Department of Anatomy I, Fujita Health University School of Medicine, Toyoake, Aichi 470-1192, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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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