Transcription Factor HUB1 Represses Sp1-Mediated Gene Expression through the CACCC Box of HTLV-I U5RE but not the GC Box
スポンサーリンク
概要
- 論文の詳細を見る
Human T-cell leukemia virus type IU5 repressive element binding protein 1 (HTLV-I U5RE Binding protein 1 ; HUB1 and renamed ZNF282) - a member of the Kruppel type zinc finger family - represses HTLV-I long terminal repeat (LTR)-mediated transcription by binding to the TCCACCC motif of the U5RE. Spl and other Spl family proteins also recognize the CACCC box of the U5RE, as well as the GC box (GGGCGG). We would therefore expect HUB1 to compete with Spl for binding to the former. In the present study, we demonstrated that Sp1 activates transcription via the U5RE, and that HUB1 represses these Sp1-mediated effects. Electrophoretic mobility shift assays (EMSA) confirmed that HUB1 was bound to the CACCC box, but not the GC box. Consistent with that finding, overexpression of HUB1 repressed Sp1-mediated transcription reporter genes controlled via the CACCC box, but not via the GC box. These results suggest that, by binding to the CACCC box, HUB1 represses the Spl-dependent transcriptional activation.
- 公益社団法人日本薬学会の論文
- 2004-08-01
著者
-
Sakata Tsuneaki
Shionogi Institute For Medical Science
-
Sakata Tsuneaki
Shionogi Discovery Research Laboratories Shionogi Co. Ltd.
-
Okumura K
Shionogi Institute For Medical Science:(present Address)ludwing Institute For Cancer Research Univer
-
IGARASHI Hisanaga
Shionogi Institute for Medical Science, Shionogi & Co., Ltd.
-
Tamura Takahiko
Shionogi Institute for Medical Science
-
Okumura Koichi
Shionogi Institute for Medical Science
-
Igarashi Hisanaga
Shionogi Institute For Medical Science
関連論文
- Serologic Evidence That Streptococcal Superantigens Are Not Involved in the Pathogenesis of Kawasaki Disease
- Transcription Factor HUB1 Represses Sp1-Mediated Gene Expression through the CACCC Box of HTLV-I U5RE but not the GC Box
- WBN/Kob-Ht Rats Spontaneously Develop Dermatitis under Conventional Conditions : Another Possible Model for Atopic Dermatitis