| First Author | Hasegawa Y | Year | 2007 |
| Journal | Biochem Biophys Res Commun | Volume | 362 |
| Issue | 4 | Pages | 988-94 |
| PubMed ID | 17803964 | Mgi Jnum | J:125187 |
| Mgi Id | MGI:3757813 | Doi | 10.1016/j.bbrc.2007.08.085 |
| Citation | Hasegawa Y, et al. (2007) Loss of ICAT gene function leads to arrest of ureteric bud branching and renal agenesis. Biochem Biophys Res Commun 362(4):988-94 |
| abstractText | 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. |
