- 著者
- Yang Weiwen Itoh Fumiko Ohya Hirotoshi Kishimoto Fukiko Tanaka Aya Nakano Naoko Itoh Susumu Kato Mitsuyasu
- 出版者
- Wiley-Blackwell
- 雑誌
- Cancer science (ISSN:13479032)
- 巻号頁・発行日
- vol.102, no.10, pp.1808-1814, 2011-10
- 被引用文献数
- 8 2
he basic helix–loop–helix protein E2-2 is known to play a role in quiescence of endothelial cells (ECs). However, it is unclear how the activity of E2-2 is controlled in the cells. In this study, we identified FAM96B as an interaction partner of E2-2. FAM96B interfered with E2-2-mediated effects on luciferase reporter activities. Furthermore, the suppression of vascular endothelial growth factor receptor 2 promoter activity by E2-2 was rescued by the expression of FAM96B in a dose-dependent manner. Interestingly, FAM96B decreased the expression of ectopic and endogenous E2-2 proteins. Mutational analysis revealed that the middle region of FAM96B is required for the limited expression of E2-2 protein. When FAM96B was expressed in ECs, the EC migration, proliferation, and tube formation were potentiated. Taken together, these findings suggest that FAM96B acts as a regulator of E2-2 through the control of its protein expression.