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2016 Fiscal Year Final Research Report

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

Research Project

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Project/Area Number 26460580
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Immunology
Research InstitutionOsaka 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

URL: 

Published: 2018-03-22  

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