Novel molecular mechanism collaborating stem neural stem cell mainteinance and differentiation

2016 Fiscal Year Final Research Report

• Project/Area Number: 26440112
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Developmental biology
• Research Institution: Shiga University of Medical Science (2015-2016); Tohoku University (2014)
• Principal Investigator: Katsuyama Yu 滋賀医科大学, 医学部, 教授 (10359862)
• Co-Investigator(Renkei-kenkyūsha): IGARASHI Kazuhiko 東北大学, 医学研究科, 教授 (00250738) ; OBAYASHI Takeshi 東北大学, 情報科学研究科, 准教授 (50397048)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 神経幹細胞

Outline of Final Research Achievements

We prepared polyclonal antibodies against Sbno1 protein, Western blot analysis using these antibodies detected different band pattern, suggesting that Sbno1 protein is regulated by cleavage. Sbno1 knockout mice showed premature neuronal differentiation, extinction of the neural stem cells, and apoptosis. Yeast two hybrid screening identified several molecules interacting with Sbno1. Our analyses suggested that one of these is transcription factor regulating cell differentiation, some of these are involved in regulation of cell cycle, and rest of these is deubiquitination enzyme which downregulates apoptosis. These findings suggest that Sbno1 function is regulated after protein translation, probably by protein cleavage mechanisms. Sbno1 can bind to multiple factors of different function, such as regulation of cell differentiation, cell cycle, and apoptosis. Thus, Sbno1 is a molecule which integrates these cellular processes.

Free Research Field

幹細胞生物学