The yeast SIN3 gene product negatively regulates the activity of the human progesterone receptor and positively regulates the activities of GAL4 and the HAP1 activator.
The yeast SIN3 gene product negatively regulates the activity of the human progesterone receptor and positively regulates the activities of GAL4 and the HAP1 activator.
复制标题
酵母SIN3基因产物负向调节人孕酮受体的活性，正向调节GAL4和HAP1激活剂的活性。
DOI：
10.1007/bf00297279
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Tsai,MJ
中科院分区：
文献类型：
--
作者：
Nawaz,Z;Baniahmad,C;Burris,TP;Stillman,DJ;O'Malley,BW;Tsai,MJ
The activation of gene transcription in eukaryotic organisms is regulated by sequence-specific DNA-binding proteins as well as by non-DNA-binding proteins. In this report we describe the modulatory functions of a non-DNA-binding protein, SIN3 (also known as SDI1, UME4, RPD1, and GAM2) on the transactivation properties of the human progesterone receptor (hPR), GAL4, and the HAPl activator in yeast. Our data suggest that SIN3 is a dual function protein. It negatively regulates the transcriptional activities of hPR-A and hPR-B by affecting the N-terminal activation domain (AFI). SIN3 positively regulates the transcriptional activities of GAL4 and the HAP1 activator. However, it has no effect on the transcriptional activities of the human glucocorticoid receptor (hGR) and GCN4. The SIN3 protein contains four copies of a paired amphipathic helix (PAH) motif. Deletion analysis of theSIN3PAH motifs shows that the PAH3 motif is essential forSIN3-mediated regulation of hPR, GAL4, and the HAPI activator. In constrast, the PAH 1, PAH2, and PAH4 motifs are not required forSIN3-mediated regulation of these activators. Additionally, we examined the mechanism(s) by which the SIN3 protein modulate the activities of various activators. We are unable to demonstrate the direct interaction of SIN3 protein with these activators using the yeast two-hybrid system or co-immunoprecipitation. These data suggest that SIN3 regulates the transactivation functions of hPR, GAL4, and the HAP1 activator by an indirect mechanism.
