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2015 Fiscal Year Final Research Report

Molecular basis of metabolic reprogramming by chromatin conversion

Planned Research

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Project AreaCrosstalk of transcriptional control and energy pathways by hub metabolites
Project/Area Number 23116009
Research Category

Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)

Allocation TypeSingle-year Grants
Review Section Biological Sciences
Research InstitutionKumamoto University

Principal Investigator

NAKAO MITSUYOSHI  熊本大学, 発生医学研究所, 教授 (00217663)

Project Period (FY) 2011-04-01 – 2016-03-31
Keywords代謝調節 / クロマチン / 遺伝子発現 / リジン脱メチル化 / フラビン / 脂肪細胞 / 癌細胞
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.

Free Research Field

分子遺伝学

URL: 

Published: 2017-05-10  

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