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由GC盒结合转录因子BTEB激活人类免疫缺陷病毒1型长末端重复序列

Activation of the human immunodeficiency virus type 1 long terminal repeat by BTEB, a GC box-binding transcription factor.

作者信息

Imataka H, Mizuno A, Fujii-Kuriyama Y, Hayami M

机构信息

Institute for Virus Research, Kyoto University, Japan.

出版信息

AIDS Res Hum Retroviruses. 1993 Sep;9(9):825-31. doi: 10.1089/aid.1993.9.825.

DOI:10.1089/aid.1993.9.825
PMID:8257632
Abstract

BTEB, a GC box-binding transcription factor, was tested for its ability to activate the human immunodeficiency virus type 1 long terminal repeat (HIV-1 LTR). An electrophoretic mobility shift assay demonstrated specific binding of BTEB to GC boxes of the HIV-1 LTR. When a BTEB expression vector was cotransfected into A3.01 cells with a fusion gene of HIV-1 LTR and chloramphenicol acetyltransferase (CAT) structural gene, the CAT activity was increased. This increase was accompanied by an increase in the content of CAT mRNA. Transcriptional activity of the HIV-1 LTR, stimulated by Tat, was further enhanced by the expression of BTEB. BTEB also activated the LTR activity in cooperation with phorbol 12-myristate 13-acetate. Northern blot analysis showed that various T cell and macrophage/monocyte cell lines expressed the BTEB mRNA to a level comparable with that of Sp1, another GC box-binding transcription factor. These results suggest that BTEB, like Sp1, is involved in transcriptional activation of the HIV-1 LTR.

摘要

BTEB是一种与GC盒结合的转录因子,我们检测了它激活人类免疫缺陷病毒1型长末端重复序列(HIV-1 LTR)的能力。电泳迁移率变动分析表明BTEB能与HIV-1 LTR的GC盒特异性结合。当将BTEB表达载体与HIV-1 LTR和氯霉素乙酰转移酶(CAT)结构基因的融合基因共转染到A3.01细胞中时,CAT活性增加。这种增加伴随着CAT mRNA含量的增加。由Tat刺激的HIV-1 LTR的转录活性,通过BTEB的表达进一步增强。BTEB还与佛波酯12-肉豆蔻酸酯13-乙酸酯协同激活LTR活性。Northern印迹分析表明,各种T细胞和巨噬细胞/单核细胞系表达BTEB mRNA的水平与另一种与GC盒结合的转录因子Sp1相当。这些结果表明,BTEB与Sp1一样,参与HIV-1 LTR的转录激活。

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