The negative regulatory mechanism of PFTR on the function of nuclear receptors

• Main Authors: Ou Yi-Hung, 歐奕宏
• Other Authors: Lee Sheng-Chung
• Format: Others
• Language: en_US
• Published: 2001
• Online Access: http://ndltd.ncl.edu.tw/handle/91540102370590143094

碩士 === 國立臺灣大學 === 生化科學研究所 === 89 === TIF1beta has been demonstrated to interact with C/EBPbeta and glucocorticioid receptor (GR) to induce AGP gene expression. TIF1beta is a PHD finger-containing protein. It’s believed that PHD-fingers are protein-protein interaction domains. They recognize a set of similar nuclear targets implicated in chromatin structure organization and regulation. In order to know whether any factor with PHD finger could interact with GR functionally, PFTR, a novel PHD finger-containing, was cloned by our lab. Recombinant GST-PFTR could interact with GR in the pull down experiment. In this thesis, I demonstrated that PFTR interacts with estrogen receptor (ER) as well as progesterone receptor (PR) physically. Furthermore, PFTR represses transcriptional activity of PR and ER in a dose-dependent manner. We also found that PFTR also represses the SRC-3-enhanced transcriptional activity of ER.