Prion protein overexpress induces on autophagy mechanism explication.
Project/Area Number |
25870474
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Pathological medical chemistry
Neurology
|
Research Institution | The University of Tokushima |
Principal Investigator |
YANO Masashi 徳島大学, 疾患酵素学研究センター, 技術員 (10531858)
|
Project Period (FY) |
2013-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | プリオン / オートファジー |
Outline of Final Research Achievements |
Prion is the disease to which neurodegeneration death happens by surplus accumulation of prion protein. The mechanism of this nerve cell death is unclear, but participation of apoptosis through autophagy is advocated. In this study, I worked on mechanism of activation of the autophagy which happens by the thing which makes a HEK293T cells protein overexpress. It's analyzed using a prion model mice whether this mechanism by HEK293T cells participates in nerve cell death of prion.
|
Report
(3 results)
Research Products
(1 results)
-
[Journal Article] Mouse-hamster chimeric prion protein (PrP) devoid of N-terminal residues 23-88 restores susceptibility to 22L prions, but not to RML prions in PrP-knockout mice.2014
Author(s)
Uchiyama K, Miyata H, Yano M, Yamaguchi Y, Imamura M, Muramatsu N, Das NR, Chida J, Hara H, Sakaguchi S.
-
Journal Title
PLoS One
Volume: 9
Issue: 10
Pages: e109737-e109737
DOI
Related Report
Peer Reviewed / Open Access