| Project/Area Number |
16K18392
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Neurochemistry/Neuropharmacology
|
|---|
| Research Institution | Nagoya University |
|---|
Principal Investigator |
TSUBOI DAISUKE 名古屋大学, 医学系研究科, 特任助教 (80584672)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
KAIBUCHI KOZO 名古屋大学, 大学院医学系研究科, 教授 (00169377)
|
|---|
| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
|
|---|
| Keywords | DISC1 / 統合失調症 / ミクログリア / サイトカイン |
|---|
| Outline of Final Research Achievements |
In this study, I identified more than 50 of DISC1-interactors by mass spectrometry, I focused on the physiological interaction of DISC1 with TRAF6. I found that DISC1 bound to TRAF6 in vitro and in vivo and that TRAF6 was delocalized in the microglia cells derived from Disc1-deficient mice. These results suggested that DISC1 was involved in intracellular signal transduction related to stress response and innate immunity through localization control of TRAF complex. In addition, to evaluate the glial cell specific DISC1 physiological function, I generated a Disc1-conditional knockout mouse. Based on Genome PCR and mRNA expression experiments, Disc1 gene deficiency was confirmed Cre-dependent. Furthermore, by mating with Cre mice expressing microglial cells specifically, cell type specific Disc1-deficient mice are being established.
|
