Transcriptional co-activator activity of SYT is negatively regulated by BRM and Brg1

被引:20
|
作者
Ishida, M
Tanaka, S
Ohki, M
Ohta, T
机构
[1] Natl Canc Ctr, Res Inst, Ctr Med Genom, Chuo Ku, Tokyo 1040045, Japan
[2] Hokkaido Univ, Sch Med, Lab Mol & Cellular Pathol, Kita Ku, Sapporo, Hokkaido 0608638, Japan
关键词
D O I
10.1111/j.1356-9597.2004.00737.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The t(X;18)(p11.2;q11.2) translocation found in synovial sarcomas results in the fusion of the SYT gene on chromosome 18 to the SSX gene on chromosome X. Although the SYT-SSX fusion proteins may trigger synovial sarcoma development, the biological functions of SYT, SSX and SYT-SSX genes are unclear. Transfections of Gal4 DNA binding domain fusion protein constructs demonstrate that SYT protein acts as a transcriptional co-activator at the C-terminal domain and that the activity is repressed through the N-terminus. The N-terminal 70 amino acids of SYT bind not only to BRM, but also to Brg1, both of which are subunits of SWI/SNF chromatin remodelling complexes. Here, we have investigated the functions of BRM and Brg1 on the repression of SYT activity. The negative regulation of SYT transcriptional co-activator activity is dependent on the ATP-hydrolysis of BRM and Brg1 in the protein complexes. This indicates that the SWI/SNF protein complexes regulate SYT activity using the chromatin remodelling activity.
引用
收藏
页码:419 / 428
页数:10
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