Transcriptional Coactivator PC4 Stimulates Promoter Escape and Facilitates Transcriptional Synergy by GAL4-VP16
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- Aya Fukuda
- Department of Molecular Biology, Saitama Medical School, Moroyama, Iruma-gun, Saitama 350-0495, Japan
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- Tomoyoshi Nakadai
- Department of Molecular Biology, Saitama Medical School, Moroyama, Iruma-gun, Saitama 350-0495, Japan
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- Miho Shimada
- Department of Molecular Biology, Saitama Medical School, Moroyama, Iruma-gun, Saitama 350-0495, Japan
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- Tohru Tsukui
- Department of Molecular Biology, Saitama Medical School, Moroyama, Iruma-gun, Saitama 350-0495, Japan
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- Masahito Matsumoto
- Department of Molecular Biology, Saitama Medical School, Moroyama, Iruma-gun, Saitama 350-0495, Japan
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- Yasuhisa Nogi
- Department of Molecular Biology, Saitama Medical School, Moroyama, Iruma-gun, Saitama 350-0495, Japan
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- Michael Meisterernst
- Gene Expression, Institute of Molecular Immunology, GSF-National Research Center for Environment and Health, Munich, Germany
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- Koji Hisatake
- Department of Molecular Biology, Saitama Medical School, Moroyama, Iruma-gun, Saitama 350-0495, Japan
書誌事項
- 公開日
- 2004-07-01
- 権利情報
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- https://journals.asm.org/non-commercial-tdm-license
- DOI
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- 10.1128/mcb.24.14.6525-6535.2004
- 公開者
- Informa UK Limited
説明
Positive cofactor 4 (PC4) is a coactivator that strongly augments transcription by various activators, presumably by facilitating the assembly of the preinitiation complex (PIC). However, our previous observation of stimulation of promoter escape in GAL4-VP16-dependent transcription in the presence of PC4 suggested a possible role for PC4 in this step. Here, we performed quantitative analyses of the stimulatory effects of PC4 on initiation, promoter escape, and elongation in GAL4-VP16-dependent transcription and found that PC4 possesses the ability to stimulate promoter escape in response to GAL4-VP16 in addition to its previously demonstrated effect on PIC assembly. This stimulatory effect of PC4 on promoter escape required TFIIA and the TATA box binding protein-associated factor subunits of TFIID. Furthermore, PC4 displayed physical interactions with both TFIIH and GAL4-VP16 through its coactivator domain, and these interactions were regulated distinctly by PC4 phosphorylation. Finally, GAL4-VP16 and PC4 stimulated both initiation and promoter escape to similar extents on the promoters with three and five GAL4 sites; however, they stimulated promoter escape preferentially on the promoter with a single GAL4 site. These results provide insight into the mechanism by which PC4 permits multiply bound GAL4-VP16 to attain synergy to achieve robust transcriptional activation.
収録刊行物
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- Molecular and Cellular Biology
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Molecular and Cellular Biology 24 (14), 6525-6535, 2004-07-01
Informa UK Limited
