| Co-Investigator(Renkei-kenkyūsha) |
IRITANI Shuji 名古屋大学, 大学院医学系研究科, 寄付講座教授 (60191904)
IIDAKA Tetsuya 名古屋大学, 脳とこころの研究センター, 教授 (70324366)
Branko Aleksic 名古屋大学, 大学院医学系研究科, 特任准教授 (60547511)
HIRAKAWA Akihiro 東京大学, 大学院医学系研究科, 特任准教授 (90609330)
NODA Yukihiro 名城大学, 薬学部, 教授 (90397464)
|
|---|
| Budget Amount *help |
¥83,330,000 (Direct Cost: ¥64,100,000、Indirect Cost: ¥19,230,000)
Fiscal Year 2017: ¥13,650,000 (Direct Cost: ¥10,500,000、Indirect Cost: ¥3,150,000)
Fiscal Year 2016: ¥13,650,000 (Direct Cost: ¥10,500,000、Indirect Cost: ¥3,150,000)
Fiscal Year 2015: ¥13,650,000 (Direct Cost: ¥10,500,000、Indirect Cost: ¥3,150,000)
Fiscal Year 2014: ¥13,650,000 (Direct Cost: ¥10,500,000、Indirect Cost: ¥3,150,000)
Fiscal Year 2013: ¥28,730,000 (Direct Cost: ¥22,100,000、Indirect Cost: ¥6,630,000)
|
|---|
| Outline of Final Research Achievements |
We performed genomic analysis of schizophrenia, autism spectrum disorders (ASD) and bipolar disorder, identified variants strongly contributing to onset in RTN4R and CX3CR1 genes, and clarified their biological significance. RTN4R p.R292H mutation caused attenuation of interacting with its partner molecule LINGO-1 from in vitro functional analysis and revealed that it affected the formation of growth cones in elongating neurons (Kimuta et al., Translational Psychiatry, 2017). In addition, we also clarified that CX3CR1 p.A55T mutation caused structural instability by attenuating interaction with lipid molecules, and inhibited PI3K/Akt/mTOR signaling pathway (Ishizuka et al., Translational Psychiatry, 2017).
|
