Analysis of non-coding RNA regulatory mechanism in B cell terminal differentiation

2016 Fiscal Year Final Research Report

• Project/Area Number: 26460580
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Immunology
• Research Institution: Osaka University (2015-2016); Kumamoto University (2014)
• Principal Investigator: Maeda Kazuhiko 大阪大学, 微生物病研究所, 准教授 (20332869)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 抗体 / 体細胞突然変異 / RNA代謝 / 非コードRNA

Outline of Final Research Achievements

Antibodies responsible for adaptive immunity have a variety of repertoires against diverse antigens. Although antibody-producing B cells differentiate into either memory B cells or plasma cells from germinal center B cells, however, it is not clear what kind of mechanism maintains antibody production ability for a long time period. In this process, a molecular regulation mechanism via activation-induced cytidine deaminase (AID), which is specifically expressed in mature B cells, is essential. In this research, we focused on GANP molecule, which is relevant to the protein, DNA and RNA level as a cofactor of AID, and it was possible to clarify the access genomic region and the GANP binding various mRNA/miRNA. From the results of this research, we could disclose the molecular basis of intracellular RNA controlled by GANP.

Free Research Field

免疫学