| Budget Amount *help |
¥42,900,000 (Direct Cost: ¥33,000,000、Indirect Cost: ¥9,900,000)
Fiscal Year 2019: ¥13,260,000 (Direct Cost: ¥10,200,000、Indirect Cost: ¥3,060,000)
Fiscal Year 2018: ¥14,040,000 (Direct Cost: ¥10,800,000、Indirect Cost: ¥3,240,000)
Fiscal Year 2017: ¥15,600,000 (Direct Cost: ¥12,000,000、Indirect Cost: ¥3,600,000)
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| Outline of Final Research Achievements |
We focused on the metabolism, activation, and intracellular function of BBF2H7 and OASIS, that are endoplasmic reticulum stress sensors, and analyzed the details of the physiological roles they have. 1) We found that small peptide derived from BBF2H7 is produced in response to ER stress, and the peptide is easy to aggregate, suggesting that the proteolysis of BBF2H7 dependent on ER stress may be involved in the pathogenesis of neurodegenerative diseases. 2) p21 was identified as a transcription target of OASIS, which was proven to be a cellular senescence-promoting factor. We succeeded in developing a new cancer treatment strategy to stop the cell growth of cancer cells by epigenome editing of oasis gene that was methylated at its promoter region. 3) The mucopolysaccharide-causing molecule IDS is degraded by ERAD pathway. Folding of mutant IDS was promoted through activation of calnexin cycle by blocking the ERAD pathway and the activities of mutant IDS was found to be recovered.
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