Role of INTS6 in the adipose differentiation

INTS6 在脂肪分化中的作用

• 批准号: 24659445
• 负责人: ASANO Tomoichiro
• 金额: $ 2.41万
• 依托单位: Hiroshima University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Challenging Exploratory Research
• 财政年份: 2012
• 资助国家: 日本
• 起止时间: 2012-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-24659445/
• 关键词: ＩＮＴＳ６; 脂肪細胞; 代謝; 分化; 肥満; INTS6; 糖尿病; 代謝調節; インスリン抵抗性; ＩＮＴＳ６; 脂肪細胞; 代謝; 分化; 肥満; INTS6; 糖尿病; 代謝調節; インスリン抵抗性

We demonstrated that expression levels ofIntS6 and IntS11, subunits ofthe Integrator complex, were increased in 3T3-L1 cells in the period when the cells reach edconfluenceand differentiated into adipocytes, while being reduced tobasal levels after the completion ofdifferentiation. Suppre ssion of IntS6 or IntS11 expression using siRNAs in3T3-L1 pre-adipocytes markedly inhibited differentiation into mature adipocytes. These findings demonstrate that increased expression of Integrator complex subunits is an indispensable event in adipose differentiation. Although further study is necessary to elucidate the underlying mechanism, the processing of U1, U2 small nuclear RNAs may be involved in cell differentiation steps.

我们证明，在细胞到达脂肪细胞中，在3T3-L1细胞中，在3T3-L1细胞中增加了Ints6和Ints11的表达水平，在3T3-L1细胞中增加了，同时降低了差异后的脂肪细胞。使用siRNAS IN3T3-L1预脂肪细胞显着抑制成熟脂肪细胞的分化，对INTS6或INTS11表达进行了反感。这些发现表明，集成剂复合亚基的表达增加是脂肪分化中必不可少的事件。尽管需要进一步的研究来阐明潜在机制，但是U1的加工U2小核RNA可能参与细胞分化步骤。