| First Author | Kamura K | Year | 2018 |
| Journal | Biochem Biophys Res Commun | Volume | 505 |
| Issue | 3 | Pages | 951-957 |
| PubMed ID | 30309656 | Mgi Jnum | J:270942 |
| Mgi Id | MGI:6276785 | Doi | 10.1016/j.bbrc.2018.10.037 |
| Citation | Kamura K, et al. (2018) Obesity in Yap transgenic mice is associated with TAZ downregulation. Biochem Biophys Res Commun 505(3):951-957 |
| abstractText | Obesity is characterized by an expansion of white adipose tissue (WAT) mass, which mainly consists of adipocytes. During the commitment and differentiation of adipocytes, PPARgamma functions as a key transcriptional factor for adipogenesis, and is associated with its suppressive coregulator, TAZ. Previous studies have shown the importance of TAZ in adipogenesis using an in vitro model; however, the understanding of its role in adipogenesis in vivo remains limited. Here, we report a unique obese mouse model that is associated with TAZ downregulation, which arose from the overexpression of Yap, a Taz paralog. YAP activation facilitated Hippo signaling feedback, which induced a compensatory reduction in YAP, subsequently neutralizing its functional activity. This feedback also induced TAZ suppression and exclusion from the nucleus. In Yap transgenic mice, TAZ downregulation in adipose stem cells activated PPARgamma, leading to their differentiation into mature adipocytes and consequently increased adipose tissue. These results highlight the in vivo necessity of TAZ for adipocyte commitment and differentiation, which could provide insight into anti-obesity therapeutics. |
