Functional analysis of atg8 homologues in developing axons
Project/Area Number |
21800048
|
Research Category |
Grant-in-Aid for Research Activity Start-up
|
Allocation Type | Single-year Grants |
Research Field |
Nerve anatomy/Neuropathology
|
Research Institution | Keio University |
Principal Investigator |
NISHIYAMA Jun Keio University, 医学部, 助教 (60508084)
|
Project Period (FY) |
2009 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥3,224,000 (Direct Cost: ¥2,480,000、Indirect Cost: ¥744,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,664,000 (Direct Cost: ¥1,280,000、Indirect Cost: ¥384,000)
|
Keywords | オートファジー / 神経細胞死 / 軸索変性 / 神経変性疾患 / 軸策変性 / 興奮毒性 / 神経発生 / 軸策形成 |
Research Abstract |
LC3, a only known marker for autophagosomes, were accumulated within developing axons. Interestingly, electron microscopical analysis reveals that there were no induction of autophagy in LC3 accumulated region, indicating that LC3 could have specific functions other than those in autophagy. Whereas, autophagy was remarkably induced in axons by intracellular ATP reduction and AMPK activation in lurcher-induced neurodegeneration. In addition, genetic suppression of autophagy significantly exacerbated Lurcher-induced neurodegeneration. These observations highlighted the cell-protective role of autophagy in neurodegeneration and modification and activation of the autophagic pathway could allow us to develop a new therapeutic approach to various neurodegenerative disorders involving excitotoxic mode of cell death.
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Report
(3 results)
Research Products
(12 results)