The role of PRMT1 signal on immune response and immune related disease
Project/Area Number |
24590286
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General physiology
|
Research Institution | Tokyo Medical University |
Principal Investigator |
HATA KIKUMI 東京医科大学, 医学部, 講師 (30287156)
|
Co-Investigator(Kenkyū-buntansha) |
TAKADA Eiko 東京医科大学, 医学部, 講師 (50110903)
|
Project Period (FY) |
2012-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | アルギニンメチル化 / 抗体産生 / タンパク質修飾 / T細胞依存性抗体産生 / PRMT1 / 国際情報交換 |
Outline of Final Research Achievements |
Protein arginine methyltransferase 1 (PRMT1), a major PRMT in mammalian cells, has been shown to play a crucial role in multiple biological functions in vitro. To explore the role of PRMT1 in B cells in vivo, we generated B cell-specific PRMT1-deficient (Prmt1-/-) mice using a Cre-loxP system. The Prmt1-/- mice showed a defect in B cell development with diminished levels of serum antibodies. Specific antibody response in Prmt1-/- mice was absent following stimulation with the type 2 T cell independent antigen NP-Ficoll but intact with the T cell-dependent antigen NP-OVA. Our finding is the first evidence that PRMT1 is necessary for lymphocyte functions in vivo.
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Report
(5 results)
Research Products
(4 results)