The role of AIM in immuno-inflammation
Project/Area Number |
15K08525
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Immunology
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Research Institution | Kyushu University (2016-2017) The University of Tokyo (2015) |
Principal Investigator |
SAKATA DAIJI 九州大学, 生体防御医学研究所, 助教 (70456870)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 免疫 / 炎症 / 神経免疫炎症 / 神経変性疾患 / アトピー / アルツハイマー / 痒み / アトピー性皮膚炎 / IL-31 / DOCKファミリー / 病態モデルマウス / DOCKファミリー分子 / DOCK8 / 病態モデル / 異物除去 / 免疫炎症 / AIM |
Outline of Final Research Achievements |
To clarify the role of AIM (Apoptosis inhibitor of macrophage) in neuroimmuno-inflammation, we established a mouse model of Alzheimer disease (AD). As a model of human AD, we generated APP (amyloid precursor protein) transgenic mice which have 4 different mutations on human APP gene (the mutations are originally seen in some types of human AD patients), and confirmed that those mice have Aβ accumulation in their brain. We expect that those mice should be a strong tool for analyzing roles of AIM in AD pathology.
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Report
(4 results)
Research Products
(3 results)
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[Journal Article] DOCK1 inhibition suppresses cancer cell invasion and macropinocytosis induced by self-activation Rac1P29S mutation.2018
Author(s)
Tomino T, Tajiri H, Tatsuguchi T, Shirai T, Oisaki K, Matsunaga S, Sanematsu F, Sakata D, Yoshizumi T, Maehara Y, Kanai M, Cote JF, Fukui Y, Uruno T
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Journal Title
Biochem.Biophys.Res.Commun.
Volume: 497
Issue: 1
Pages: 298-304
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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