Interference of E2-2-mediated effect in endothelial cells by FAM96B through its limited expression of E2-2 Interference of E2-2-mediated effect in endothelial cells by FAM96B through its limited expression of E2-2

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Author(s)

    • YANG Weiwen
    • Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences, University of Tsukuba
    • ITOH Fumiko
    • Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences, University of Tsukuba
    • OHYA Hirotoshi
    • Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences, University of Tsukuba
    • KISHIMOTO Fukiko
    • Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences, University of Tsukuba
    • TANAKA Aya
    • Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences, University of Tsukuba
    • NAKANO Naoko
    • Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences, University of Tsukuba
    • ITOH Susumu
    • Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences, University of Tsukuba
    • KATO Mitsuyasu
    • Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences, University of Tsukuba

Abstract

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.

Journal

  • Cancer science

    Cancer science 102(10), 1808-1814, 2011-10-10

    Wiley-Blackwell

References:  31

Keywords

Codes

  • NII Article ID (NAID)
    10030243800
  • NII NACSIS-CAT ID (NCID)
    AA11808050
  • Text Lang
    ENG
  • Article Type
    ART
  • ISSN
    13479032
  • Data Source
    CJP  IR 
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