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D型cyclin、E2F-1、SV40 large T antigen と HPV16 E7の大量発現によるCCG1/TAFII250の変異によるtsBN462細胞の細胞周期停止の抑制：関口猛^1,2、西本毅治²、トニー　ハンター¹ (¹,ソーク研究所分子生物ウイルス、²,九大医分子生命)

Overexpression of D-type cyclins, E2F-1, SV40 large T antigen and HPV16 E7 rescue cell cycle arrest of tsBN462 cells casued by CCG1/TAFII250 mutation: Takeshi SEKIGUCHI^1,2, Takeharu NISHIMOTO² and Tony HUNTER¹(¹,Molecular Biology and Virology Laboratory, The Salk Institute,U.S.A. ²,Department of Molecular Biology, Graduate School of Medical Science, Kyushu University)

TsBN462 cells, which have a point mutation in CCG1/TAFII250, a component of TFIID complex, arrest in G1 at the nonpermissive temperature of 39.5。C. Overexpression of D-type cyclins rescued the cell cycle arrest of tsBN462 cells, suggesting that the cell cycle arrest was through Rb. Consistent with this, overexpression of E2F-1, whose function is repressed by the nonphosphorylated form of Rb, also rescued the cell cycle arrest. Moreover, expression of the viral oncoproteins SV40 large T antigen and HPV16 E7, which both bind Rb and inactivate its function, rescued the cell cycle arrest, whereas HPV16 E6 did not. Mutation of the Rb-binding motif in E7 abrogated its ability to rescue the cell cycle arrest. Expression of exogenous cyclin D1, SV40 large T antigen or CCG1/TAFII250 increased cyclin A expression at 39.5。C. To investigate the mechanism underlying the lack of cyclin D1 expression, deletion analysis of cyclin D1 promoter was performed. The 0.15 kbp cyclin D1 core promoter region that lacks any transcription factor binding motifs still exhibited a temperature-sensitive phenotype in tsBN462 cells suggesting that CCG1/TAFII250 is critical for the function of the cyclin D1 core promoter.