Epigenetic transcriptional master regulator for hematopoietic cell differentiation

造血细胞分化的表观遗传转录主调节因子

• 批准号: 22790335
• 负责人: SUZUKI Mitsuhiro
• 金额: $ 2.5万
• 依托单位: University of Occupational and Environmental Health, Japan
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22790335/
• 关键词: 血球分化; 転写調節; 発生・分化; エピジェネティクス; 血球細胞

Transcription factor PU. 1 is a hematopoietic master regulator and essential for the development of myeloid and B-cell lineages. PU. 1 functions in concert with other transcription factors and cofactors. As we shown previously represented, PU. 1 interact with both p300/cbp, which function as a coactivator and HDAC, which function as a corepressor. In this study, to determine whether modification of PU. 1 is responsible for switching its association between coactivaor and corepressor, we examined whether acetylation regulates the physical and functional activities of PU. 1.We found that PU. 1 was acetylated in vivo and its repressor activity was reduced when the putative acetylation motif in ETS domain were mutated. Our data suggest that acetylation might regulate the biological functions in erythroid cells.

转录因子PU。1是造血主调节因子，并且对于骨髓和B细胞谱系的发育是必需的。PU. 1与其他转录因子和辅因子一起发挥作用。如前所述，PU。1与p300/cbp和HDAC相互作用，p300/cbp起辅激活剂的作用，HDAC起辅抑制剂的作用。在本研究中，以确定是否改性聚氨酯。1负责在辅激活子和辅抑制子之间转换其缔合，我们研究了乙酰化是否调节PU的物理和功能活性。1.我们找到了PU。1在体内被乙酰化，突变ETS结构域中的乙酰化基序可降低其阻遏活性。我们的数据表明，乙酰化可能调节红系细胞的生物学功能。

项目成果

Hypoxia induces CD133 expression in human lung cancer cells by up-regulation of OCT3/4 and SOX2

• DOI: 10.3892/ijo.2011.1207
• 发表时间: 2012-01-01
• 期刊: INTERNATIONAL JOURNAL OF ONCOLOGY
• 影响因子: 5.2
• 作者: Iida, Hajime;Suzuki, Mitsuhiro;Ueno, Hikaru
• 通讯作者: Ueno, Hikaru