| Budget Amount *help |
¥122,330,000 (Direct Cost : ¥94,100,000、Indirect Cost : ¥28,230,000)
Fiscal Year 2015 : ¥23,140,000 (Direct Cost : ¥17,800,000、Indirect Cost : ¥5,340,000)
Fiscal Year 2014 : ¥23,140,000 (Direct Cost : ¥17,800,000、Indirect Cost : ¥5,340,000)
Fiscal Year 2013 : ¥24,440,000 (Direct Cost : ¥18,800,000、Indirect Cost : ¥5,640,000)
Fiscal Year 2012 : ¥24,180,000 (Direct Cost : ¥18,600,000、Indirect Cost : ¥5,580,000)
Fiscal Year 2011 : ¥27,430,000 (Direct Cost : ¥21,100,000、Indirect Cost : ¥6,330,000)
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| Outline of Final Research Achievements |
Epigenetic marks such as methylation of DNA and histones are stably maintained or dynamically changed for gene regulation. The epigenetic states may be reprogrammed by environmental stimuli and inherited as the cellular memory. In fact, epigenetic alteration of disease-related genes is implicated in metabolic diseases and cancer. This study showed that the lysine demethylase LSD1, a nuclear enzyme which utilizes the flavin adenosine dinucleotide (FAD) as a cofactor, regulates energy metabolism in mouse adipocytes. Our data suggest that FAD-dependent demethylation by LSD1 suppresses energy expenditure genes under obese condition. Further, we found that overexpressed LSD1 changes the balance of oxidative phosphorylation and glycolysis in cancer cells, and that LSD2, another family member, works for protecting lipotoxicity in hepatic cells. These indicate that the LSD1 family proteins have an essential role in metabolic reprogramming in various cell types.
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