| Budget Amount *help |
¥21,060,000 (Direct Cost: ¥16,200,000、Indirect Cost: ¥4,860,000)
Fiscal Year 2020: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2019: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2018: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
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| Outline of Final Research Achievements |
In this study, we tested the hypothesis that disruption of the membrane contact region between the endoplasmic reticulum and mitochondria (ER-mitochondrial intermembrane region; MAM) is a general pathogenesis in amyotrophic lateral sclerosis (ALS). We generated a novel reporter molecule named MAMtracker and demonstrated that the MAM is disrupted by various ALS-causing genes. Furthermore, we found that MAM disruption significantly reduces the activity of TANK-binding kinase 1 (TBK1), which is also the causative gene product of ALS, and that this is due to impaired stress-dependent MAM-specific ubiquitination. This study will provide the basis for future development of MAM-targeted ALS therapies.
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