| First Author | Peng Y | Year | 2011 |
| Journal | J Biol Chem | Volume | 286 |
| Issue | 46 | Pages | 40331-42 |
| PubMed ID | 21949185 | Mgi Jnum | J:178154 |
| Mgi Id | MGI:5297624 | Doi | 10.1074/jbc.M111.302059 |
| Citation | Peng Y, et al. (2011) The Leucine Zipper Putative Tumor Suppressor 2 Protein LZTS2 Regulates Kidney Development. J Biol Chem 286(46):40331-42 |
| abstractText | Members of the leucine zipper putative tumor suppressor (LZTS) family play crucial roles in transcription modulation and cell cycle control. We previously demonstrated that LZTS2 functions as a novel beta-catenin-interacting protein and represses beta-catenin-mediated transcription on T-cell factor/lymphoid enhancing factor. Here, we investigate the biological role of LZTS2 using newly established Lzts2 KO mice. Homozygosity for loss-of-function of the Lzts2-targeted allele resulted in severe kidney and urinary tract developmental defects, including renal/ureteral duplication, hydroureter, and hydronephrosis, which were visible prenatally. Altered ureteric bud outgrowth was identified in Lzts2 null embryos. Further analysis indicated that beta-catenin subcellular localization was altered in fibroblasts isolated from Lzts2 null embryos. In addition, Wnt growth factor-induced beta-catenin-mediated transcriptional activity was increased in Lzts2 null fibroblasts, suggesting a direct role for Lzts2 in the Wnt signaling pathway. These data demonstrate a critical role of LZTS2 in renal development and implicate LZTS2 as a critical regulator of beta-catenin-mediated nephrogenesis. |
